ArticleScientific reports2017
Protein tyrosine phosphatase Shp2 deficiency in podocytes attenuates lipopolysaccharide-induced proteinuria.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- CDKAL1 dysfunction impairs lysine codon translation in podocytes and accelerates chronic kidney disease.The EMBO journal · 2026Article
- Mapping of PTP1B, TCPTP, SHP2, and Putative Substrates Reveals Novel Networks in Glomerular Podocytes.Journal of cellular physiology · 2026Article
- Protein tyrosine phosphatase 1B is a regulator of alpha-actinin4 in the glomerular podocyte.Biochimica et biophysica acta. Molecular cell research · 2024Article
- SHP2 regulates adipose maintenance and adipocyte-pancreatic cancer cell crosstalk via PDHA1.Journal of cell communication and signaling · 2023Article
- SHP2: its association and roles in systemic lupus erythematosus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Deficiency of the Src homology phosphatase 2 in podocytes is associated with renoprotective effects in mice under hyperglycemia.Cellular and molecular life sciences : CMLS · 2022Article
- Pulmonary surfactants and the respiratory-renal connection in steroid-sensitive nephrotic syndrome of childhood.iScience · 2022Article
- Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin.Cell communication and signaling : CCS · 2022Article
- Adiponectin receptor agonist AdipoRon ameliorates renal inflammation in diet-induced obese mice and endotoxin-treated human glomeruli ex vivo.Diabetologia · 2021Article
- Phosphatases in toll-like receptors signaling: the unfairly-forgotten.Cell communication and signaling : CCS · 2021Review
- SHP2 inhibitor PHPS1 ameliorates acute kidney injury by Erk1/2-STAT3 signaling in a combined murine hemorrhage followed by septic challenge model.Molecular medicine (Cambridge, Mass.) · 2020Article
- MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Proteinuric Kidney Diseases: A Podocyte's Slit Diaphragm and Cytoskeleton Approach.Frontiers in medicine · 2018Review
- Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury.Metabolism: clinical and experimental · 2017Article
- Soluble epoxide hydrolase in podocytes is a significant contributor to renal function under hyperglycemia.Biochimica et biophysica acta. General subjects · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Podocytes are specialized epithelial cells that play a significant role in maintaining the integrity of the glomerular filtration barrier and preventing urinary protein leakage. We investigated the contribution of protein tyrosine phosphatase Shp2 to lipopolysaccharide (LPS)-induced renal injury. We report increased Shp2 expression in murine kidneys and cultured podocytes following an LPS challenge. To determine the role of podocyte Shp2 in vivo, we generated podocyte-specific Shp2 knockout (pod-Shp2 KO) mice. Following administration of LPS, pod-Shp2 KO mice exhibited lower proteinuria and blood urea nitrogen concentrations than controls indicative of preserved filter integrity. In addition, renal mRNA and serum concentrations of inflammatory cytokines IL-1β, TNFα, INFγ and IL-12 p70 were significantly decreased in LPS-treated knockout mice compared with controls. Moreover, the protective effects of podocyte Shp2 deficiency were associated with decreased LPS-induced NF-κB and MAPK activation, nephrin phosphorylation and attenuated endoplasmic reticulum stress. These effects were recapitulated in differentiated E11 murine podocytes with lentiviral-mediated Shp2 knockdown. Furthermore, Shp2 deficient podocytes displayed reduced LPS-induced migration in a wound healing assay. These findings identify Shp2 in podocytes as a significant contributor to the signaling events following LPS challenge and suggest that inhibition of Shp2 in podocytes may present a potential therapeutic target for podocytopathies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.