Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney malformations are common causes of chronic renal failure in children. Dysplastic kidneys represent a unique model of perturbed epithelial-mesenchymal interaction which leads to the formation of malformed branching tubules surrounded by undifferentiated and metaplastic mesenchymal cells. We have found that human dysplastic epithelia express PAX2 (a transcription factor), BCL2 (a survival factor) and galectin-3 (a cell adhesion/signaling molecule). These genes are implicated in oncogenesis and their persistent expression may drive proliferation of dysplastic cysts, hence explaining the massive growth of some multicystic dysplastic kidneys. We have also detected prominent apoptosis in undifferentiated tissues around dysplastic epithelia, and this may provide a potential mechanism for the well-documented regression of dysplastic kidneys. Hence, although these kidneys may not have any excretory function, it is incorrect to consider them as 'end stage organs' because they are highly active in terms of cell turnover and gene expression; furthermore, these processes can be correlated with patterns of tissue growth and involution. Further elucidation of 'molecular lesions' in renal malformations may lead to novel therapies to enhance the differentiation of progenitor cells.
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PMID:Gene expression and cell turnover in human renal dysplasia. 1066 6

Human mesenchymal stromal cells (hMSCs) were injected into the hippocampus of adult mice 1 day after transient global ischemia. The hMSCs both improved neurologic function and markedly decreased neuronal cell death of the hippocampus. Microarray assays indicated that ischemia up-regulated 586 mouse genes. The hMSCs persisted for <7 days, but they down-regulated >10% of the ischemia-induced genes, most of which were involved in inflammatory and immune responses. The hMSCs also up-regulated three mouse genes, including the neuroprotective gene Ym1 that is expressed by activated microglia/macrophages. In addition, the transcriptomes of the hMSC changed with up-regulation of 170 human genes and down-regulation of 54 human genes. Protein assays of the hippocampus demonstrated increased expression in microglia/macrophages of Ym1, the cell survival factor insulin-like growth factor 1, galectin-3, cytokines reflective of a type 2 T cell immune bias, and the major histocompatibility complex II. The observed beneficial effects of hMSCs were largely explained by their modulation of inflammatory and immune responses, apparently by alternative activation of microglia and/or macrophages.
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PMID:Stem/progenitor cells from bone marrow decrease neuronal death in global ischemia by modulation of inflammatory/immune responses. 1879 23

In this study, we found that expression and secretion of galectin-3 (GAL-3) were upregulated by amyloid-beta42 (Abeta42) exposure in human umbilical cord blood-derived mesenchymal stem cell (hUCB-MSC) without cell death. Abeta42-exposed rat primary cortical neuronal cells co-treated with recombinant GAL-3 were protected from neuronal death in a dose-dependent manner. hUCB-MSCs were cocultured with Abeta42-exposed rat primary neuronal cells or the neuroblastoma cell line, SH-SY5Y in a Transwell chamber. Coculture of hUCB-MSCs reduced cell death of Abeta42-exposed neurons and SH-SY5Y cells. This neuroprotective effect of hUCB-MSCs was reduced significantly by GAL-3 siRNA. These data suggested that hUCB-MSC-derived GAL-3 is a survival factor against Abeta42 neurotoxicity.
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PMID:Galectin-3 secreted by human umbilical cord blood-derived mesenchymal stem cells reduces amyloid-beta42 neurotoxicity in vitro. 2065 11