RGS7 silence protects palmitic acid-induced pancreatic β-cell injury by inactivating the chemokine signaling pathway

Abstract

Impaired insulin secretion due to pancreatic β-cell injury is an important cause of type 2 diabetes (T2D). Regulators of guanine nucleotide binding protein (G protein) signaling proteins played a key role in regulating insulin sensitivity in vivo. To explore the role of RGS7 on palmitic acid-induced pancreatic β-cell injury, pancreatic β-cells Beta-TC-6 and Min6 were treated with palmitic acid (PA) to similar type 2 diabetes (T2D) injury in vitro. The 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT), 5-ethynyl-2′-deoxyuridine (EdU), and flow cytometry were used to analyze cell viability, proliferation, and apoptosis, respectively. Enzyme-linked immunosorbent assay (ELISA) kits were used to analyze the changes of inflammation-related cytokines. The expression of gene and protein was measured by quantitative real-time PCR (qRT-PCR) and western blot. PA modeling induced apoptosis, increased levels of inflammation-related cytokines, and suppressed cell viability and proliferation of pancreatic β-cells. RGS7 silence markedly alleviated the cell injury induced by PA. RGS7 overexpression further aggravated apoptosis and inflammatory response in PA-induced pancreatic β-cells and inhibited cell viability and proliferation. It is worth noting that RGS7 activated the chemokine signaling pathway. Silence of the key gene of the chemokine signaling pathway could eliminate the negative effect of RGS7 on PA-induced pancreatic β-cells. RGS7 silence protects pancreatic β-cells from PA-induced injury by inactivating the chemokine signaling pathway.

Keywords:

• RGS7
• diabetes
• pancreatic β-cells
• chemokine signaling pathway
• apoptosis

Acknowledgments

Not applicable

Author contributions

Conception and design: Yurong Zhu; Experiment: Yurong Zhu, Jun Li and Tao Ba; Data analysis and interpretation: Yuan Sun and Xiangyun Chang; Manuscript writing: Yurong Zhu; Final approval of manuscript: All authors

Ethics approval and Consent to participate

No animal and patients

Consent for publication

Not Applicable.

Disclosure statement

The authors declare that they have no conflicts of interest.

Availability of data and material

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

Additional information

Funding

This study was supported by National Natural Science Foundation of China (81860149) and University-level scientific research project (ZZZC202073A).