Insulin-like growth factor-1 inhibits apoptosis of rat gastric smooth muscle cells under high glucose condition via adenosine monophosphate-activated protein kinase (AMPK) pathway

Zhang, Xiang-Zi; Sun, Yanan; Zhang, Mohan; Jin, Zheng

doi:10.5603/fhc.a2022.0005

Cited by 3 publications

(3 citation statements)

References 41 publications

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“…These findings suggested that IGF1 is the vital activator of RORα in early bone repair. It is well known that adenosine monophosphate‐activated protein kinase (AMPK) and mitogen‐activated protein kinase (MAPK) pathways are the classical downstream intracellular signal pathways of IGF1, 24 , 25 so we tested whether IGF1 regulated the expression of RORα by these two pathways. AMPK activator AICAR promoted phosphorylation of AMPK and RORα expression in THP‐1 cells (Figure 4I,J ).…”

Section: Resultsmentioning

confidence: 99%

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Targeting RORα in macrophages to boost diabetic bone regeneration

et al. 2023

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Diabetes mellitus (DM) has become a serious threat to human health. Bone regeneration deficiency and nonunion caused by DM is perceived as a worldwide epidemic, with a very high socioeconomic impact on public health. Here, we find that targeted activation of retinoic acid‐related orphan receptor α (RORα) by SR1078 in the early stage of bone defect repair can significantly promote in situ bone regeneration of DM rats. Bone regeneration relies on the activation of macrophage RORα in the early bone repair, but RORα of DM rats fails to upregulation as hyperglycemic inflammatory microenvironment induced IGF1‐AMPK signalling deficiency. Mechanistic investigations suggest that RORα is vital for macrophage‐induced migration and proliferation of bone mesenchymal stem cells (BMSCs) via a CCL3/IL‐6 depending manner. In summary, our study identifies RORα expressed in macrophages during the early stage of bone defect repair is crucial for in situ bone regeneration, and offers a novel strategy for bone regeneration therapy and fracture repair in DM patients.

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Section: Resultsmentioning

confidence: 99%

“…It is well known that adenosine monophosphate-activated protein kinase (AMPK) and mitogen-activated protein kinase (MAPK) pathways are the classical downstream intracellular signal pathways of IGF1, 24,25…”

Section: Insufficient Igf1-ampk Signalling Of Dm Rats Blocks Upregula...mentioning

confidence: 99%

Targeting RORα in macrophages to boost diabetic bone regeneration

et al. 2023

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“…Available data on the role of AMPK in the regulation of apoptosis are controversial. While some reports suggest AMPK-dependent stimulation of apoptosis [ 39 , 40 , 41 ], several studies demonstrate an anti-apoptotic role of AMPK [ 22 , 42 , 43 , 44 ].…”

Section: Discussionmentioning

confidence: 99%

AMPK Phosphorylation Impacts Apoptosis in Differentiating Myoblasts Isolated from Atrophied Rat Soleus Muscle

Vilchinskaya

Rozhkov

Turtikova

et al. 2023

Cells

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Regrowth of atrophied myofibers depends on muscle satellite cells (SCs) that exist outside the plasma membrane. Muscle atrophy appears to result in reduced number of SCs due to apoptosis. Given reduced AMP-activated protein kinase (AMPK) activity during differentiation of primary myoblasts derived from atrophic muscle, we hypothesized that there may be a potential link between AMPK and susceptibility of differentiating myoblasts to apoptosis. The aim of this study was to estimate the effect of AMPK activation (via AICAR treatment) on apoptosis in differentiating myoblasts derived from atrophied rat soleus muscle. Thirty rats were randomly assigned to the following two groups: control (C, n = 10) and 7-day hindlimb suspension (HS, n = 20). Myoblasts derived from the soleus muscles of HS rats were divided into two parts: AICAR-treated cells and non-treated cells. Apoptotic processes were evaluated by using TUNEL assay, RT-PCR and WB. In differentiating myoblasts derived from the atrophied soleus, there was a significant decrease (p < 0.05) in AMPK and ACC phosphorylation in parallel with increased number of apoptotic nuclei and a significant upregulation of pro-apoptotic markers (caspase-3, -9, BAX, p53) compared to the cells derived from control muscles. AICAR treatment of atrophic muscle-derived myoblasts during differentiation prevented reductions in AMPK and ACC phosphorylation as well as maintained the number of apoptotic nuclei and the expression of pro-apoptotic markers at the control levels. Thus, the maintenance of AMPK activity can suppress enhanced apoptosis in differentiating myoblasts derived from atrophied rat soleus muscle.

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A. officinarum Hance – P. cablin (Blanco) Benth drug pair improves oxidative stress, intracellular Ca2+ concentrations and apoptosis by inhibiting the AGE/RAGE axis to ameliorate diabetic gastroparesis: In vitro and in vivo studies

Zheng,

Xue,

Wang

et al. 2024

Journal of Ethnopharmacology

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Insulin-like growth factor-1 inhibits apoptosis of rat gastric smooth muscle cells under high glucose condition via adenosine monophosphate-activated protein kinase (AMPK) pathway

Abstract: This article has been peer reviewed and published immediately upon acceptance.It is an open access article, which means that it can be downloaded, printed, and distributed freely, provided the work is properly cited. Articles in "Folia Histochemica et Cytobiologica" are listed in PubMed.

Cited by 3 publications

References 41 publications

Targeting RORα in macrophages to boost diabetic bone regeneration

Targeting RORα in macrophages to boost diabetic bone regeneration

AMPK Phosphorylation Impacts Apoptosis in Differentiating Myoblasts Isolated from Atrophied Rat Soleus Muscle

A. officinarum Hance – P. cablin (Blanco) Benth drug pair improves oxidative stress, intracellular Ca2+ concentrations and apoptosis by inhibiting the AGE/RAGE axis to ameliorate diabetic gastroparesis: In vitro and in vivo studies

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