ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
Transcription factor old astrocyte specifically induced substance is a novel regulator of kidney fibrosis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
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- The Regulatory Network of CREB3L1 and Its Roles in Physiological and Pathological Conditions.International journal of medical sciences · 2024Review
- Knockdown of lncRNA MALAT1 attenuates renal interstitial fibrosis through miR-124-3p/ITGB1 axis.Scientific reports · 2023Article
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- Single-cell multiomics reveals the complexity of TGFβ signalling to chromatin in iPSC-derived kidney organoids.Communications biology · 2022Article
- Upregulation of OASIS/CREB3L1 in podocytes contributes to the disturbance of kidney homeostasis.Communications biology · 2022Article
- CXCL10 is a novel anti-angiogenic factor downstream of p53 in cardiomyocytes.Physiological reports · 2022Article
- Identification of biomarkers of chronic kidney disease among kidney-derived proteins.Clinical proteomics · 2022Article
- Roles of Ceramides in Non-Alcoholic Fatty Liver Disease.Journal of clinical medicine · 2021Review
- Transcription factor old astrocyte specifically induced substance is a novel regulator of kidney fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Single-Cell and Bulk Transcriptome Data Integration Reveals Dysfunctional Cell Types and Aberrantly Expressed Genes in Hypertrophic Scar.Frontiers in genetics · 2021Article
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Prevention of kidney fibrosis is an essential requisite for effective therapy in preventing chronic kidney disease (CKD). Here, we identify Old astrocyte specifically induced substance (OASIS)/cAMP responsive element-binding protein 3-like 1 (CREB3l1), a CREB/ATF family transcription factor, as a candidate profibrotic gene that drives the final common pathological step along the fibrotic pathway in CKD. Although microarray data from diseased patient kidneys and fibrotic mouse model kidneys both exhibit OASIS/Creb3l1 upregulation, the pathophysiological roles of OASIS in CKD remains unknown. Immunohistochemistry revealed that OASIS protein was overexpressed in human fibrotic kidney compared with normal kidney. Moreover, OASIS was upregulated in murine fibrotic kidneys, following unilateral ureteral obstruction (UUO), resulting in an increase in the number of OASIS-expressing pathological myofibroblasts. In vitro assays revealed exogenous TGF-β1 increased OASIS expression coincident with fibroblast-to-myofibroblast transition and OASIS contributed to TGF-β1-mediated myofibroblast migration and increased proliferation. Significantly, in vivo kidney fibrosis induced via UUO or ischemia/reperfusion injury was ameliorated by systemic genetic knockout of OASIS, accompanied by reduced myofibroblast proliferation. Microarrays revealed that the transmembrane glycoprotein Bone marrow stromal antigen 2 (Bst2) expression was reduced in OASIS knockout myofibroblasts. Interestingly, a systemic anti-Bst2 blocking antibody approach attenuated kidney fibrosis in normal mice but not in OASIS knockout mice after UUO, signifying Bst2 functions downstream of OASIS. Finally, myofibroblast-restricted OASIS conditional knockouts resulted in resistance to kidney fibrosis. Taken together, OASIS in myofibroblasts promotes kidney fibrosis, at least in part, via increased Bst2 expression. Thus, we have identified and demonstrated that OASIS signaling is a novel regulator of kidney fibrosis.
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