ArticleNaunyn-Schmiedeberg's archives of pharmacology2013
Protective role of growth hormone against hyperhomocysteinemia-induced glomerular injury.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Catalpol inhibits HHcy-induced EndMT in endothelial cells by modulating ROS/NF-κB signaling.BMC cardiovascular disorders · 2024Article
- Omega-3FAs Can Inhibit the Inflammation and Insulin Resistance of Adipose Tissue Caused by HHcy Induced Lipids Profile Changing in Mice.Frontiers in physiology · 2021Article
- (Pro)renin receptor contributes to renal mitochondria dysfunction, apoptosis and fibrosis in diabetic mice.Scientific reports · 2019Article
- Article
- Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Protective Action of Anandamide and Its COX-2 Metabolite against l-Homocysteine-Induced NLRP3 Inflammasome Activation and Injury in Podocytes.The Journal of pharmacology and experimental therapeutics · 2016Article
- (Pro)renin receptor regulates autophagy and apoptosis in podocytes exposed to high glucose.American journal of physiology. Endocrinology and metabolism · 2015Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The present study investigated the protective role of growth hormone (GH) against hyperhomocysteinemia (hHcys)-induced activations of reactive oxygen species/hypoxia-inducible factor (HIF)-1α, epithelial-mesenchymal transition (EMT), and consequent glomerular injury. A hHcys model was induced by folate free diet in mice. The urine protein excretion significantly increased while plasma GH levels dramatically decreased in hHcys. Real-time reverse transcription polymerase chain reaction showed that GH receptor (GHR) level increased in the cortex of hHcys mice, which mainly occurred in podocytes as shown by confocal microscopy. Recombinant mouse growth hormone (rmGH) treatment (0.02 mg/kg, once a day for 6 weeks) significantly restored the plasma GH, inhibited GHR upregulation and attenuated proteinuria. Correspondingly, rmGH treatment also blocked hHcys-induced decrease in the expression of podocin, a podocyte slit diaphragm molecule, and inhibited the increases in the expression of desmin, a podocyte injury marker. It was also demonstrated that in hHcys the expression of epithelial markers, p-cadherin and ZO-1, decreased, while the expression of mesenchymal markers, antifibroblast-specific protein 1 (FSP-1) and α-SMA, increased in podocytes, which together suggest the activation of EMT in podocytes. Nicotinamide adenine dinucleotide phosphate oxidase (Nox)-dependent superoxide anion (O2 (.-)) and hypoxia-inducible factor-1α (HIF-1α) level in the hHcys mice cortex was markedly enhanced. These hHcys-induced EMT enhancement and Nox-dependent O2 (.-)/HIF-1α activation were significantly attenuated by rmGH treatment. HIF-1α level increased in Hcys-treated cultured podocytes, which were blocked by rmGH treatment. Meanwhile, homocysteine (Hcys)-induced EMT in cultured podocytes was significantly reversed by HIF-1α siRNA. All these results support the view that GH ameliorates hHcys-induced glomerular injury by reducing Nox-dependent O2 (.-)/HIF-1α signal pathway and EMT.
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Registered trials
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