Bioactive biodegradable polycitrate nanoclusters enhances the myoblast differentiation and in vivo skeletal muscle regeneration via p38 MAPK signaling pathway

Abstract Background Muscle development is a precisely orchestrated and complex process, and circular RNAs (circRNAs) has been demonstrated to play important roles in skeletal muscle growth and development. However, the regulatory functions of circRNA during buffalo muscle developmental processes have not been understood.Results In this study, Ribo-Zero RNA-Seq was performed to investigate the circRNAs expression profiles of proliferated and differentiated buffalo myoblasts. A stringent set of 3,142 circRNAs was finally characterized. Comparing the expression profiles of circRNAs revealed that 110 circRNAs were expressed differentially during myoblast differentiation. We focused on the role of a candidate circRNA, which was named circPICALM based on its host gene PICALM, and was highly (but differentially) expressed in proliferated and differentiated myoblasts. Flow cytometry, EdU incorporation, and Western blotting assays demonstrate that circPICALM promoted myoblasts proliferation and inhibited cells apoptosis. Moreover, overexpression of circPICALM promoted the differentiation of primary buffalo myoblasts. Moreover, circPICALM in vivo stimulated skeletal muscle regeneration in cardiotoxin-induced muscle injury. The RNA pulldown results showed that circPICALM could capture TUBA1B protein, revealing that circPICALM might exert its biological function by binding TUBA1B protein. Conclusions These results demonstrate that the novel non-coding regulator circPICALM induces myoblast differentiation and skeletal muscle regeneration.

Download Full-text

Perfluorooctanoic acid disrupts the blood–testis barrier and activates the TNFα/p38 MAPK signaling pathway in vivo and in vitro

Archives of Toxicology ◽

10.1007/s00204-015-1492-y ◽

2015 ◽

Vol 90 (4) ◽

pp. 971-983 ◽

Cited By ~ 37

Author(s):

Yin Lu ◽

Bin Luo ◽

Jing Li ◽

Jiayin Dai

Keyword(s):

Signaling Pathway ◽

P38 Mapk ◽

Perfluorooctanoic Acid ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Blood Testis Barrier

Download Full-text

Gga-miR-3525 Targets PDLIM3 through the MAPK Signaling Pathway to Regulate the Proliferation and Differentiation of Skeletal Muscle Satellite Cells

International Journal of Molecular Sciences ◽

10.3390/ijms21155573 ◽

2020 ◽

Vol 21 (15) ◽

pp. 5573

Author(s):

Huadong Yin ◽

Jing Zhao ◽

Haorong He ◽

Yuqi Chen ◽

Yan Wang ◽

...

Keyword(s):

Skeletal Muscle ◽

Growth Rate ◽

Signaling Pathway ◽

P38 Mapk ◽

Satellite Cells ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Muscle Satellite Cells ◽

Skeletal Muscle Satellite Cells ◽

Proliferation And Differentiation

MicroRNAs (miRNAs) are evolutionarily conserved, small noncoding RNAs that post-transcriptionally regulate expression of their target genes. Emerging evidence demonstrates that miRNAs are important regulators in the development of skeletal muscle satellite cells (SMSCs). Our previous research showed that gga-miR-3525 is differentially expressed in breast muscle of broilers (high growth rate) and layers (low growth rate). In this study, we report a new role for gga-miR-3525 as a myogenic miRNA that regulates skeletal muscle development in chickens. Exogenous increases in the expression of gga-miR-3525 significantly inhibited proliferation and differentiation of SMSCs, whereas the opposite effects were observed in gga-miR-3525 knockdown SMSCs. We confirmed that PDLIM3 (PDZ and LIM domain 3) is a target gene of gga-miR-3525 that can promote proliferation and differentiation of SMSCs. We found that PDLIM3 overexpression elevated the abundance of phosphorylated (p-)p38 protein but that the gga-miR-3525 mimic and p38-MAPK inhibitor (SB203580) weakened the activation of p-p38. Furthermore, treatment with SB203580 reduced the promoting effect of PDLIM3 on SMSC proliferation and differentiation. Overall, our results indicate that gga-miR-3525 regulates the proliferation and differentiation of SMSCs by targeting PDLIM3 via the p38/MAPK signaling pathway in chickens.

Download Full-text

LncRNA CCAT1 Enhances Chemoresistance in Hepatocellular Carcinoma by Targeting QKI-5

10.21203/rs.3.rs-60542/v1 ◽

2020 ◽

Author(s):

Jing Shi ◽

Cao Guo ◽

Junli Ma

Keyword(s):

Hepatocellular Carcinoma ◽

Drug Resistance ◽

Signaling Pathway ◽

P38 Mapk ◽

Tumor Model ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Promising Alternative

Abstract Background: A major reason for treatment failure of cancer is acquisition of drug resistance. The specific mechanisms underlying hepatocellular carcinoma (HCC) chemoresistance need to be fully elucidated. lncRNAs involve in drug resistance in some cancers, however, the exact functions of lncRNA colon cancer-associated transcript 1 (CCAT1) in oxaliplatin resistance in HCC need to be elucidated.Methods: Functional analysis of CCAT1 on oxaliplatin sensitivity was performed in HCC cell lines HCCLM3 and HepG2, and in a subcutaneous tumor model receiving OXA treatment. Furthermore, the downstream signaling targets of CCAT1 in HCC were explored. Results: CCAT1 promoted HCC proliferation and reduced the apoptosis induced by oxaliplatin. Knockout of CCAT1 could increased chemosensitivity in vitro and in vivo. Further study found that QKI-5 was an important mediator and blocking of QKI-5/p38 MAPK signaling pathway enhanced oxaliplatin sensitivity.Conclusions: CCAT1 promoted proliferation and oxaliplatin resistance by QKI-5/p38 MAPK signaling pathway in HCC. Targeting CCAT1 in combination with chemotherapeutics may be a promising alternative to reverse drug resistance in HCC treatment.

Download Full-text

Attenuation of High Glucose-Induced Damage in RPE Cells through p38 MAPK Signaling Pathway Inhibition

Frontiers in Pharmacology ◽

10.3389/fphar.2021.684680 ◽

2021 ◽

Vol 12 ◽

Author(s):

Grazia Maugeri ◽

Claudio Bucolo ◽

Filippo Drago ◽

Settimio Rossi ◽

Michelino Di Rosa ◽

...

Keyword(s):

Signaling Pathway ◽

P38 Mapk ◽

High Glucose ◽

Retinal Pigment ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Rpe Cells ◽

Cox 2

This study aimed to investigate the high glucose damage on human retinal pigment epithelial (RPE) cells, the role of p38 MAPK signaling pathway and how dimethyl fumarate can regulate that. We carried out in vitro studies on ARPE-19 cells exposed to physiological and high glucose (HG) conditions, to evaluate the effects of DMF on cell viability, apoptosis, and expression of inflammatory and angiogenic biomarkers such as COX-2, iNOS, IL-1β, and VEGF. Our data have demonstrated that DMF treatment attenuated HG-induced apoptosis, as confirmed by reduction of BAX/Bcl-2 ratio. Furthermore, in RPE cells exposed to HG we observed a significant increase of iNOS, COX-2, and IL-1β expression, that was reverted by DMF treatment. Moreover, DMF reduced the VEGF levels elicited by HG, inhibiting p38 MAPK signaling pathway. The present study demonstrated that DMF provides a remarkable protection against high glucose-induced damage in RPE cells through p38 MAPK inhibition and the subsequent down-regulation of VEGF levels, suggesting that DMF is a small molecule that represents a good candidate for diabetic retinopathy treatment and warrants further in vivo and clinical evaluation.

Download Full-text