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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 235 records · Page 13
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

MiR-502 mediates esophageal cancer cell TE1 proliferation by promoting AKT phosphorylation

Esophageal cancer is one of the most common cancers in the world and esophageal squamous cell carcinoma is one of the two main types in esophageal cancer. MicroRNA is a small non-coding RNA molecule functions in many different cancers including esophageal cancer. We found miR-502 was up-regulated in esophageal tissues, which indicated miRNA-502 may play important roles in esophageal cancer. In this study, we used esophageal cancer cell line TE1 as an in vitro model for investigating the role of miR-502 in promoting the proliferation of the cancer cells. We found that overexpressing miR-502 in TE1 cells promoted the proliferation and inhibited the apoptosis induced by dox. Down-regulating miR-502 made the opposite phenomenon. Furthermore, western blot showed that miR-502 enhanced the phosphorylation levels of AKT pathways, which may be the mechanism of the overgrowth for esophageal cancer cell. Our data provide the evidence of a role for miR-502 in the regulation the proliferation of esophageal cancer cell through promoting the phosphorylation of AKT signaling. Due to its ability to promote the overgrowth of esophageal cancer cell, miR-502 may be a novel target for esophageal cancer therapeutic.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

The role of lncRNA XIST/miR-211 axis in modulating the proliferation and apoptosis of osteoarthritis chondrocytes through CXCR4 and MAPK signaling

Long noncoding RNAs (lncRNAs) participate in multiple diverse diseases, including osteoarthritis (OA). Here, we explored the role of lncRNA XIST in OA and identified the potential molecular mechanisms. The expression of XIST in cartilage samples in patients with OA was significantly upregulated. XIST knockdown remarkably suppressed IL-1β-suppressed OA chondrocyte proliferation while promoted IL-1β-induced cell apoptosis. By employing online tools, miRNAs related to CXCR4, a major contributor to chondrocyte apoptosis, and XIST were selected. miR-211 expression could be significantly inhibited by IL-1β stimulation, and miR-211 negatively regulated XIST expression and CXCR4 protein levels. Through direct binding, XIST served as a ceRNA for miR-211 to counteract miR-211-mediated CXCR4 repression, thereby modulating chondrocyte proliferation and apoptosis through downstream MAPK signaling. In OA tissues, miR-211 expression was significantly downregulated while CXCR4 mRNA expression was upregulated. miR-211 was negatively correlated with XIST and CXCR4, respectively, while XIST and CXCR4 was positively correlated in tissue samples. In conclusion, the study revealed that lncRNA XIST can promote the proliferation of OA chondrocytes and promote apoptosis through the miR-211/CXCR4 axis. Thus, lncRNA XIST might be considered as a potential therapeutic target for OA treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Protein kinase C alpha-mediated phosphorylation of PIM-1L promotes the survival and proliferation of acute myeloid leukemia cells

FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) is a constitutively active mutant of FLT3 and causes 20%–30% of acute myeloid leukemia (AML) cases. FLT3-ITD upregulates the proviral integration site for Moloney murine leukemia virus 1 (PIM-1) expression and promotes the proliferation of AML cells. In this study, we investigated the role of protein kinase C (PKC)-mediated phosphorylation on the expression and function of PIM-1L. Drug screening in leukemia cell lines revealed that sotrastaurin (a PKC inhibitor) suppressed the proliferation of the FLT3-ITD-positive AML cell line MV4-11 but not of K562, HL60, or KG-1a cells, similar to SGI-1776 (a PIM-1/FLT3 inhibitor) and quizartinib (an FLT3 inhibitor). Sotrastaurin decreased the expression of pro-survival protein myeloid cell leukemia (MCL-1) and the phosphorylation of eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), both of which are downstream effectors of PIM-1. PKCα directly phosphorylated Ser65 of PIM-1L, which is a long isoform of PIM-1. The PKCα-mediated phosphorylation stabilized PIM-1L. The phosphorylation-mimicked mutant, PIM-1L-S65D, was more stable and showed higher kinase activity than PIM-1L-S65A. Expression of PIM-1L-wildtype or -S65D reduced sotrastaurin-mediated apoptosis and growth inhibition in MV4-11 transfectants. These results suggest that PKCα directly upregulates PIM-1L, resulting in promotion of the survival and proliferation of AML cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

LncRNA LINC00968 accelerates the proliferation and fibrosis of diabetic nephropathy by epigenetically repressing p21 via recruiting EZH2

Highlights: • LncRNA LINC00968 was high-expressed in the diabetic db/db mouse tissue and high-glucose induced mesangial cells. • LINC00968 silencing inhibited the proliferation and cycle progression. • LINC00968 silencing decreased the extracellular matrix (ECM) proteins (fibronectin, collagen IV) expression. • RIP and ChIP assay revealed that LINC00968 recruit EZH2 to the promoter of p21 to inhibit its expression. Emerging evidence have indicated the vital roles of long noncoding RNAs (lncRNAs) in the pathophysiological process of diabetic nephropathy. However, the deepgoing mechanism that lncRNAs regulate the diabetic nephropathy pathogenesis is still ambiguous. In present study, we found that lncRNA LINC00968 expression was high-expressed in the diabetic db/db mouse tissue and high-glucose induced mesangial cells. Functional experiments indicated that LINC00968 silencing by siRNAs significantly inhibited the proliferation and cycle progression, and decreased the extracellular matrix (ECM) proteins (fibronectin, collagen IV) expression in the high glucose induced of mesangial cells. RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assay revealed that LINC00968 recruit EZH2 to the promoter of p21 to inhibit its expression. In summary, our results support the conclusion that lncRNA LINC00968 accelerates the proliferation and fibrosis of mesangial cells by epigenetically repressing p21 via recruiting EZH2, providing a novel insight for the diabetic nephropathy pathogenesis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

CCN1 accelerates re-epithelialization by promoting keratinocyte migration and proliferation during cutaneous wound healing

Highlights: • Re-epithelialization is the restoration of skin integrity following injury. • CCN family member 1 (CCN1) is upregulated in the early stages following injury. • CCN1 promotes human primary keratinocyte migration and proliferation. • Topical CCN1 application stimulates re-epithelialization in mouse burn models. • CCN1 is more potent than bFGF in initiating re-epithelialization. Re-epithelialization is an essential part of wound healing and has a prominent influence on the prognosis. CCN family member 1 (CCN1 or Cysteine-rich 61, CYR61), a matricellular protein, has a potential role in the wound healing process. However, its role in re-epithelialization remains unclear. The aim of this study was to determine the expression of CCN1 in the epidermis and its effect on keratinocytes during re-epithelialization. CCN1 expression in the wounded skin was analyzed using microarray data from GEO database and detected by immunofluorescence. The results showed upregulated CCN1 during the early stages of wound healing. Human primary keratinocytes were treated with recombinant human CCN1. The results showed that CCN1 promoted keratinocyte migration and proliferation. Moreover, a full-thickness mouse skin wound model and a superficial second-degree burn mouse model treated intracutaneously with CCN1 were used for in vivo studies. Topical treatment with CCN1 protein accelerated wound closure and re-epithelialization. Additionally, longer newly-formed epithelium tongue and elevated expression of PCNA and Ki67 were detected in the CCN1-treated group 4 days post-burn. These results indicate that CCN1 accelerates re-epithelialization by promoting keratinocyte migration and proliferation, and may serve as a novel target to promote re-epithelialization.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Liraglutide, a glucagon-like peptide-1 receptor agonist, facilitates osteogenic proliferation and differentiation in MC3T3-E1 cells through phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), extracellular signal-related kinase (ERK)1/2, and cAMP/protein kinase A (PKA) signaling pathways involving β-catenin

Previous studies have proven that glucagon-like peptide-1 (GLP-1) and its receptor agonist exert favorable anabolic effects on skeletal metabolism. However, whether GLP-1 could directly impact osteoblast-mediated bone formation is still controversial, and the underlying molecular mechanism remains to be elucidated. Thus in this paper, we investigated the effects of liraglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, on murine MC3T3-E1 preosteoblasts proliferation and differentiation and explored the potential cellular basis. Our study confirmed the presence of GLP-1R in MC3T3-E1, and demonstrated that liraglutide promotes osteoblasts proliferation at an intermediate concentration (100 nM) and time (48 h), upregulated the expression of osteoblastogenic biomarkers at various stages, and stimulated osteoblastic mineralization. Liraglutide also elevated the intracellular cAMP level and phosphorylation of AKT, ERK and β-catenin simultaneously with increased nuclear β-catenin content and transcriptional activity. Pretreatment of cells with the inhibitors LY294002, PD98059, H89 and GLP-1R and β-catenin siRNA partially blocked the liraglutide-induced signaling activation and attenuated the facilitating effect of liraglutide on MC3T3-E1 cells. Collectively, liraglutide was capable of acting upon osteoblasts directly through GLP-1R by activating PI3K/AKT, ERK1/2, cAMP/PKA/β-cat-Ser675 signaling to promote bone formation via GLP-1R. Thus, GLP-1 analogues may be potential therapeutic strategy for the treatment of osteoporosis in diabetics. - Highlights: • Liraglutide promoted proliferation and differentiation of murine MC3T3-E1 preosteoblasts. • GLP-1R was expressed in MC3T3-E1 cells. • These effects were mediated by PI3K/AKT, ERK1/2, and cAMP/PKA pathway via GLP-1R. • β-catenin was also involved in this complex process.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

BMP-2 enhances the migration and proliferation of hypoxia-induced VSMCs via actin cytoskeleton, CD44 and matrix metalloproteinase linkage

Highlights: • BMP-2 upregulates hypoxia-induced VSMC migration. • BMP-2 reduces F-actin disaggregate. • BMP-2 increase CD44 production. • PEX inhibits MMP-2 and CD44 combining. The persistent proliferation of hypoxia-induced vascular smooth muscle cells (VSMCs) in the arterial wall underlie the development of atherosclerosis. However, the mechanism that regulates the behavior of VSMCs, which involve in actin aggregation, and impedes their migration is still elusive. Here, we report that bone morphogenetic protein 2 (BMP-2) leads to enrichment of CD44 and F-actin stress fiber and secretion of matrix metalloproteinases-2 (MMP-2) during hypoxia in vitro and following artificial hypoxia-induced atherosclerosis exacerbation in vivo. To test this hypothesis, fluorescence immunostaining, immune-hybridization and flow cytometry analyses were performed to understand the relationship among BMP-2, CD44 and MMP-2 linkage. The cellular actin cytoskeleton was reduced, and smaller adhesion plaques were formed in hypoxia-induced T/G HA-VSMC cell line, but BMP-2 against disruption of F-actin and increase the motility and migration behaviors of VSMC during hypoxic cultured. Aggregation of F-actin dependents on the interaction between the cell surface integral membrane protein CD44 and Vinculin which enhanced by rBMP-2. This activity of Actin/CD44/ linkage was inhibited by competing with the active site of the CD44 using recombined the hemopexin-like C-terminal domain (PEX) of MMP-2. These results lead to the proliferation and migration of VSMCs were inhibited in response to MMP-2 activity when the cell is in a hypoxic environment. Collectively, our discovery indicates that BMP-2 could enhance migration and proliferation of hypoxia-induced VSMCs via the Actin/CD44/MMP-2 molecular pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Hepatitis B virus promotes proliferation and metastasis in male Chinese hepatocellular carcinoma patients through the LEF-1/miR-371a-5p/SRCIN1/pleiotrophin/Slug pathway

Highlights: • miR-371a-5p is upregulated in HCC and related to HBV Infection, sexuality. • The overexpression of miR-371a-5p predicted poor overall survival. • miR-371a-5p promote the proliferation and metastasis of hepatoma cells. • miR-371a-5p is upregulated by HBV and testosterone through LEF-1. • miR-371a-5p through SRCIN1/NF-kB/PTN/Slug pathway promote the hepatocarcinogenesis. Hepatocellular carcinoma (HCC) is a male-dominant cancer. Several factors may contribute to the gender difference. Recent investigations have reported that miRNAs are involved in sex-linked signaling pathways and play a critical role in the molecular pathogenesis of hepatitis B virus (HBV)-related HCC. Therefore, we speculated that some of these miRNAs might contribute to the gender differences observed in HBV-related HCC. Our results showed that miR-371a-5p was significantly upregulated in tumor tissue and serum from HCC patients and that the expression level of miR-371a-5p was related to HBV infection, sexuality, TNM stage, adjacent organ invasion and microvascular invasion. Moreover, a high level of miR-371a-5p expression predicted poor overall survival of HCC patients, and in vitro and in vivo studies revealed that the overexpression of miR-371a-5p promoted proliferation and metastasis. Mechanistic investigations suggested that miR-371a-5p was upregulated by HBV and testosterone through LEF-1. SRCIN1 was a direct target of miR-371a-5p and reversed the effects of miR-371a-5p on HCC tumorigenesis. Our results also revealed that SRCIN1 negatively regulated the expression of PTN by inhibiting the activity of NF-κB. As a hepatocyte growth factor, PTN promoted EMT-induced metastasis in vitro and in vivo through the AKT/Slug pathway. These data strongly suggested that the upregulation of miR-371a-5p played an important role in HBV-related HCC. Through the LEF-1/miR-371a-5p/SRCIN1/PTN/Slug pathway, HBV and testosterone promote the proliferation and metastasis of hepatoma cells, especially in male patients with HBV-related HCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

miR-190 promotes HCC proliferation and metastasis by targeting PHLPP1

Highlights: • miR-190 enhances the proliferation and metastasis of HCC. • miR-190 specifically inhibits PHLPP1 expression. • miR-190 may serve as a potential target and marker for HCC treatment. miRNAs regulate gene expression and enable clinicians to distinguish between benign and malignant tissues in cancers. PH domain leucine-rich repeat-containing protein phosphatase 1 (PHLPP1) is known to be a tumour suppressor. A lentiviral overexpression system was used to stably express miR-190, leading to the enhancement of hepatocellular carcinoma (HCC) proliferation and metastasis as a result of inhibited PHLPP1 expression. The results showed that stable miR-190 expression increased the expression of EMT-related proteins (Snail and TCF8/ZEB1) as well as the phosphorylation of Akt at Ser473 and the expression of a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1). However, restoring PHLPP1 expression counteracted the effects of miR-190 on HCC proliferation, migration and invasion. The results of the animal experiments showed that miR-190 improved the HepG2 cell tumour formation and lung metastasis ability. Stable miR-190 overexpression leads to the downregulation of PHLPP1 protein expression. miR-190 has potential as a target in the treatment and diagnosis of HCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Necrosulfonamide reverses pyroptosis-induced inhibition of proliferation and differentiation of osteoblasts through the NLRP3/caspase-1/GSDMD pathway

The acute inflammatory stimulation occurring after a bone fracture regulates the repair and healing of local bone injury; however, under certain conditions, pyroptosis may occur in osteoblasts, which affects osteoblast proliferation and differentiation, thereby affecting the growth, development and morphological changes of bone tissue. The aim of the present study was to examine the effect of the pyroptosis inhibitor necrosulfonamide (NSA) on the proliferation and differentiation of osteoblasts and elucidate the underlying mechanism. The results revealed that NSA reversed the effects of ATP/lipopolysaccharide (LPS) on cell viability and pyroptosis, and on the mRNA and protein expression of pyroptosis-related genes. It also suppressed the secretion of IL-6, TNF-α and IL-1β and reversed the effects of ATP/LPS on the activity of ALP and the mRNA expression of differentiation-related genes in osteoblasts. The fact that overexpression of caspase-1, gasdermin D (GSDMD) and NLRP3 abolished the effects of NSA on the viability and pyroptosis of osteoblasts, as well as the mRNA expression of differentiation-related genes and the activity of ALP in osteoblasts, indicated that NSA promoted the proliferation and differentiation of osteoblasts by inhibiting the NLRP3/caspase-1/GSDMD pyroptosis pathway. The present study provides proof supporting the potential application of NSA for improving the function of osteoblasts in fracture repair and indicates the value of the NLRP3/caspase-1/GSDMD pyroptosis pathway as a pharmaceutical target.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Sepsis induces muscle atrophy by inhibiting proliferation and promoting apoptosis via PLK1‐AKT signalling

Abstract Sepsis and sepsis‐induced skeletal muscle atrophy are common in patients in intensive care units with high mortality, while the mechanisms are controversial and complicated. In the present study, the atrophy of skeletal muscle was evaluated in sepsis mouse model as well as the apoptosis of muscle fibres. Sepsis induced atrophy of skeletal muscle and apoptosis of myofibres in vivo and in vitro. In cell‐based in vitro experiments, lipopolysaccharide (LPS) stimulation also inhibited the proliferation of myoblasts. At the molecular level, the expression of polo‐like kinase 1 (PLK1) and phosphorylated protein kinase B (p‐AKT) was decreased. Overexpression of PLK1 partly rescued LPS‐induced apoptosis, proliferation suppression and atrophy in C2C12 cells. Furthermore, inhibiting the AKT pathway deteriorated LPS‐induced atrophy in PLK1‐overexpressing C2C12 myotubes. PLK1 was found to participate in regulating apoptosis and E3 ubiquitin ligase activity in C2C12 cells. Taken together, these results indicate that sepsis induces skeletal muscle atrophy by promoting apoptosis of muscle fibres and inhibiting proliferation of myoblasts via regulation of the PLK1‐AKT pathway. These findings enhance understanding of the mechanism of sepsis‐induced skeletal muscle atrophy.

Cao, Ying‐Ya↗
DOE OSTI2023

Application of Proliferation Resistance Optimization (PRO-X) Methodology to a Generic Research Reactor

The Proliferation Resistance Optimization Program (PRO-X) has been established by the NNSA to provide a framework for evaluating and integrating proliferation resistance into nuclear reactor system (core, fuel, and auxiliary facilities) designs that also maintain the safety and peaceful use missions of those systems. The research reactor (PRO-RR) area is the component of PRO-X that supports the program objectives by applying state-of-the-art analysis methods to research reactor systems. This report details the results of using a defined set of analytical tools to evaluate the neutronics, thermal hydraulics and proliferation risk characteristics of a set of parametric cores based on a generic 10 MW materials test reactor that uses a plate-type low enriched uranium (LEU) fuel. The analysis shows that by suitable adjustment of the core size, reflector configuration and power level, mission performance and safety margins can be maintained or improved while reducing the potential for production of special nuclear material.

22 GENERAL STUDIES OF NUCLEAR REACTORS↗
DOE OSTI2021

Artificial Judgement Assistance from teXt (AJAX): Applying Open Domain Question Answering to Nuclear Non-proliferation Analysis

Nuclear non-proliferation analysis is complex and subjective, as the data is sparse, and examples are rare and diverse. While analysing non-proliferation data, it is often desired that the findings be completely auditable such that any claim or assertion can be sourced directly to the reference material from which it was derived. Currently this is accomplished by analysts thoroughly documenting underlying assumptions and clearly referencing details to source documents. This is a labour-intensive and time-consuming process that can be difficult to scale with geometrically increasing quantities of data. In this work, we describe an approach to leverage bi-directional language models for nuclear non-proliferation analysis. It has been shown recently that these models not only capture language syntax but also some of the relational knowledge present in the training data. We have devised a unique Salt and Pepper strategy for testing the knowledge present in the language models, while also introducing auditability function in our pipeline. We demonstrate that fine-tuning the bi-directional language models on domain specific corpus improves their ability to answer domain-specific factoid questions. Our hope is that the results presented in this paper will further the natural language processing (NLP) field by introducing the ability to audit the answers provided by the language models to bring forward the source of said knowledge.

98 NUCLEAR DISARMAMENT, SAFEGUARDS, AND PHYSICAL P↗
NASA NTRS1999

Nitric oxide donors, sodium nitroprusside and S-nitroso-N-acetylpencillamine, stimulate myoblast proliferation in vitro

Nitric oxide (NO) is an inter- and intracellular messenger involved in a variety of physiologic and pathophysiologic conditions. The effect of two NO donors, sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) and their effect on myoblast proliferation was examined. Both donors stimulated an increase in myoblast cell number over a range (1-10 microM) of donor concentrations. However, 50 microM SNAP inhibited myoblast proliferation. Cell numbers from cultures treated with degraded 10 microM SNAP were equivalent to the control. Therefore, it appears NO can stimulate as well as inhibit myoblast proliferation.

Non-NASA Center↗
NASA NTRS1996

Cell proliferation and hair cell addition in the ear of the goldfish, Carassius auratus

Cell proliferation and hair cell addition have not been studied in the ears of otophysan fish, a group of species who have specialized hearing capabilities. In this study we used the mitotic S-phase marker bromodeoxyuridine (BrdU) to identify proliferating cells in the ear of one otophysan species, Carassius auratus (the goldfish). Animals were sacrificed at 3 h or 5 days postinjection with BrdU and processed for immunocytochemistry. The results of the study show that cell proliferation occurs in all of the otic endorgans and results in the addition of new hair cells. BrdU-labeled cells were distributed throughout all epithelia, including the primary auditory endorgan (saccule), where hair cell phenotypes vary considerably along the rostrocaudal axis. This study lays the groundwork for our transmission electron microscopy study of proliferative cells in the goldfish ear (Presson et al., Hearing Research 100 (1996) 10-20) as well as future studies of hair cell development in this species. The ability to predict, based on epithelial location, the future phenotype of developing hair cells in the saccule of the goldfish make that endorgan a particularly powerful model system for the investigation of early hair cell differentiation.

NASA Discipline Number 40-10↗
NASA NTRS1994

Inhibition of murine splenic T lymphocyte proliferation by 2-deoxy-D-glucose-induced metabolic stress

Female Swiss-Webster mice were injected with the glucose analogue 2-deoxy-D-glucose (2-DG), which when administered to rodents induces acute periods of metabolic stress. A single or multiple injections of 2-DG invoked a stress response, as evidenced by increases in serum corticosterone levels. The influence of this metabolic stressor on the blastogenic potential of splenic T lymphocytes was then examined. It was found that one, two, or three injections of 2-DG resulted in depressed T cell proliferative responses, with an attenuation of the effect occurring by the fifth injection. The 2-DG-induced inhibition of T cell proliferation was not attributable to 2-DG-induced cytolysis, as in vitro incubation of naive T cells with varying concentrations of 2-DG did not result in a reduction in cell number or viability, and flow cytometric analysis demonstrated that percentages of CD3, CD4, and CD8 splenic T cells were not altered as a result of 2-DG-induced stress. Incubating naive T cells in varying concentrations of 2-DG resulted in a dose-dependent inhibition of T cell blastogenic potential. Following in vivo exposure to 2-DG, T cell proliferation did not return to normal levels until 3 days after the cessation of 2-DG injections. Administering the beta-adrenergic receptor antagonist propranolol did not reverse the inhibited lymphoproliferation in 2-DG-treated mice. The inhibition in T cell proliferation was not observed, however, in mice that had been adrenalectomized or hypophysectomized and injected with 2-DG.(ABSTRACT TRUNCATED AT 250 WORDS).

Non-NASA Center↗
NASA NTRS1993

Cell proliferation and differentiation in chemical leukemogenesis

In tissues such as bone marrow with normally high rates of cell division, proliferation is tightly coordinated with cell differentiation. Survival, proliferation and differentiation of early hematopoietic progenitor cells depend on the growth factors, interleukin 3 (IL-3) and/or granulocyte-macrophage colony stimulating factor (GM-CSF) and their synergism with other cytokines. We provide evidence that a characteristic shared by a diverse group of compounds with demonstrated leukemogenic potential is the ability to act synergistically with GM-CSF. This results in an increase in recruitment of a resting population of hematopoietic progenitor cells normally unresponsive to the cytokine and a twofold increase in the size of the proliferating cell population normally regarded to be at risk of transformation in leukemogenesis. These findings support the possibility that transient alterations in hematopoietic progenitor cell differentiation may be an important factor in the early stages of development of leukemia secondary to chemical or drug exposure.

Non-NASA Center↗
NASA NTRS2006

Analysis of Cell Proliferation in Newt (Pleurodeles waltl) Tissue Regeneration during Spaceflight in Foton M-2

Terrestrial organisms exposed to microgravity during spaceflight expe rience musculoskeletal degeneration. It is still not understood if lo nger-term exposures to microgravity induce degeneration in other tiss ues, and if these effects are also observed in neutrally buoyant aqu atic organisms that may be pre-adapted to mechanical unloading. The " Regeneration" experiment conducted collaboratively between Russian an d US scientists for 16 days in the Russian Foton M-2 spaceflight soug ht to test the hypothesis that microgravity alters the proliferation of cells in regenerating tail tissue of the newt Pleurodeles waltl. Our initial results indicate that we successfUlly delivered the proli feration marker 5-bromo-2'-deoxy Uridine (BrdU) during spaceflight, and that it was incorporated in the nuclei of cells in regenerating tis sues. Cells in spaceflight tail regenerates proliferated at a slight ly slower rate and were more undifferentiated than those in ground sy nchronous controls. In addition, the size of regenerating tails from spaceflight was smaller than synchronous controls. However, onboard temperature recordings show that the temperature in spaceflight was a bout 2 C lower than ground synchronous controls, possibly explaining the observed differences. Additional post-facto ground controls at ma tched temperatures will correctly determine the effects of spaceflig ht on regenerative cell proliferation in the newt.

Almeida, E. A. C.↗