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STK11 overexpression prevents glucocorticoid-induced osteoporosis via activating the AMPK/SIRT1/PGC1α axis

Jiao Xiao1, Wenjin Li1, Guojuan Li1

  • 1Department of Endocrinology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, No.336 Dongfeng South Road, Zhuhui District, Hengyang, 421001, Hunan, China.

Human Cell
|May 11, 2022
PubMed

Insights

STK11 (serine/threonine kinase 11) activation protects against glucocorticoid-induced osteoporosis by enhancing the AMPK/SIRT1/PGC1α pathway in human mesenchymal stromal cells.

Area of Science:

  • Orthopedics
  • Cell Biology
  • Molecular Biology

Background:

  • Osteoporosis (OP) is a common orthopedic condition often caused by glucocorticoids.
  • Glucocorticoid-induced OP impairs bone health, leading to pain, fractures, and deformities.

Purpose of the Study:

  • To investigate the role and mechanism of STK11 in glucocorticoid-induced osteoporosis (OP).
  • To explore STK11's function in human mesenchymal stromal cells (hMSCs) under dexamethasone (DEX) treatment.

Main Methods:

  • Established an in-vitro OP model using DEX on hMSCs.
  • Assessed cell viability, differentiation, apoptosis, and ROS levels.
  • Utilized inhibitors and activators (SIRT1, PGC1α, AMPK) to elucidate STK11's mechanism.

Main Results:

  • STK11 expression was reduced in OP tissues and DEX-treated hMSCs.
  • STK11 overexpression counteracted DEX's inhibitory effects on osteogenic differentiation.
  • STK11 activation of the AMPK/SIRT1/PGC1α pathway was confirmed through inhibitor/activator studies.

Conclusions:

  • STK11 plays a protective role against glucocorticoid-induced OP.
  • STK11 functions by activating the AMPK/SIRT1/PGC1α signaling axis.
  • Targeting STK11 may offer a therapeutic strategy for glucocorticoid-induced osteoporosis.
Keywords:
AMPKGlucocorticoidsOsteoporosisPGC1αSIRT1STK11

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