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SOCS-1 is involved in TNF-α-induced mitochondrial dysfunction and apoptosis in renal tubular epithelial cells

Chunyang Du1, Fang Yao1, Yunzhuo Ren1

  • 1Department of Pathology and Key Laboratory of Kidney Diseases of Hebei Province, Hebei Medical University, Shijiazhuang, China.

Tissue & Cell
|July 23, 2017
PubMed

Insights

Suppressor of cytokine signaling-1 (SOCS-1) protects human renal cells from tumor necrosis factor-alpha (TNF-α)-induced damage. Overexpression of SOCS-1 reduces oxidative stress and apoptosis, potentially via the JAK/STAT pathway.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumor necrosis factor-alpha (TNF-α) may worsen kidney function in chronic kidney disease (CKD) by damaging renal tubular cells.
  • The role of suppressor of cytokine signaling-1 (SOCS-1) in TNF-α-induced renal cell injury is not fully understood.

Purpose of the Study:

  • To investigate the involvement of SOCS-1 in TNF-α-induced oxidative stress and apoptosis in human renal tubular epithelial cells (HKCs).
  • To explore the potential mechanism, including the JAK/STAT signaling pathway, by which SOCS-1 influences these processes.

Main Methods:

  • HKCs were treated with TNF-α to assess changes in SOCS-1 expression, apoptosis, and oxidative stress.
  • SOCS-1 was overexpressed in HKCs to evaluate its protective effects.
  • The JAK/STAT pathway was investigated using a JAK2 inhibitor (AG490).

Main Results:

  • TNF-α increased SOCS-1 expression, apoptosis, and activation of apoptosis signal regulating kinase-1 (ASK1) in HKCs.
  • Overexpression of SOCS-1 attenuated TNF-α-induced oxidative stress and apoptosis.
  • Inhibition of JAK2 with AG490 reduced TNF-α-induced oxidative stress and apoptosis.
  • SOCS-1 overexpression appeared to regulate the JAK/STAT signaling pathway.

Conclusions:

  • SOCS-1 plays a protective role against TNF-α-mediated oxidative stress and apoptosis in HKCs.
  • The protective mechanism of SOCS-1 may involve the suppression of JAK/STAT signaling pathway activation.
Keywords:
ApoptosisHKCMitochondrial dysfunctionSOCS-1TNF-α

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