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The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
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A decreasing function describes a relationship where the output consistently declines as the input increases. This means that for any two input values, if one is greater than the other, the corresponding output is smaller. Mathematically, a function f is decreasing on an interval I if for every x1 < x2​ in I, f (x1) > f (x2). This type of behavior is visually identified on a graph that slopes downward from left to right.The nature of a function can be analyzed by calculating...
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Decrease of GSK3β Ser-9 Phosphorylation Induced Osteoblast Apoptosis in Rat Osteoarthritis Model.

Shuang Deng1, Zhi-Gang Nie1, Pu-Ji Peng1

  • 1Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, 430060, China.

Current Medical Science
|March 15, 2019
PubMed
Summary
This summary is machine-generated.

Glucocorticoids cause osteonecrosis of the femoral head (ONFH) by inducing osteoblast apoptosis. Glycogen synthase kinase 3β (GSK3β) plays a key role, with its inhibition protecting against this cell death.

Keywords:
GSK3βapoptosisdexamethasoneosteonecrosis of the femoral headphosphorylation

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Orthopedics

Background:

  • Glucocorticoid excess is a primary cause of non-traumatic osteonecrosis of the femoral head (ONFH).
  • Osteoblast apoptosis is the key molecular mechanism underlying ONFH pathogenesis.
  • Glycogen synthase kinase 3β (GSK3β) regulates cell differentiation and apoptosis, but its role in ONFH is largely unexplored.

Purpose of the Study:

  • To investigate the role of GSK3β phosphorylation in glucocorticoid-induced ONFH.
  • To explore GSK3β as a potential therapeutic target for ONFH.

Main Methods:

  • Established a rat ONFH model using lipopolysaccharide and methylprednisolone.
  • Analyzed GSK3β phosphorylation and expression of apoptosis-related proteins (β-catenin, Bcl-2, Bax, caspase-3) via Western blotting.
  • Utilized dexamethasone (Dex) to induce apoptosis in primary osteoblasts.
  • Inhibited GSK3β expression (siRNA) and function (LiCl) in Dex-treated osteoblasts.

Main Results:

  • Decreased GSK3β phosphorylation at Ser-9 observed in the rat ONFH model.
  • Consistent alterations in GSK3β phosphorylation and apoptosis markers in Dex-incubated osteoblasts.
  • GSK3β knockdown reduced pro-apoptotic factors (Bax, cleaved caspase-3) and increased anti-apoptotic factor (Bcl-2) and β-catenin.
  • LiCl treatment counteracted Dex-induced caspase-3 activation.

Conclusions:

  • GSK3β phosphorylation is altered in ONFH.
  • GSK3β inhibition protects osteoblasts from glucocorticoid-induced apoptosis.
  • GSK3β represents a promising therapeutic target for managing ONFH.