Related Experiment Video

Updated: Jan 23, 2026

Acute Myocardial Infarction in Rats
07:45

Acute Myocardial Infarction in Rats

Published on: February 16, 2011

54.5K

Role and mechanism of microRNA-548c-3p/c-Myb in myocardial infarction fibrosis in rats

L-X Zhang1, S-H Zhang, C-Q Wang

  • 1Department of Gerontology, The Third Hospital of Hebei Medical University, Shijiazhuang, China. daylight1981@126.com.

European Review for Medical and Pharmacological Sciences
|June 19, 2019
PubMed
Abstract

Insights

MicroRNA-548c-3p upregulation improved cardiac function and reduced myocardial fibrosis after myocardial infarction. This microRNA targets c-Myb, inhibiting fibrosis-related factors.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Biochemistry

Background:

  • Myocardial infarction (MI) often leads to myocardial fibrosis, a significant cause of heart dysfunction.
  • MicroRNAs (miRNAs) play crucial roles in post-MI cardiac remodeling and fibrosis.
  • The specific role of microRNA (miR)-548c-3p in myocardial fibrosis remains largely unexplored.

Purpose of the Study:

  • To investigate the role of miR-548c-3p in myocardial fibrosis following myocardial infarction (MI).
  • To explore the underlying molecular mechanisms, including its relationship with c-Myb.

Main Methods:

  • Established a rat model of MI and used lentivirus transfection to upregulate miR-548c-3p.
  • Assessed cardiac function via echocardiography and fibrosis levels using Sirius red and Masson staining.
  • Utilized an in vitro oxygen-glucose deprivation (OGD) model with isolated myocardial fibroblasts to study miR-548c-3p and c-Myb interactions, measuring α-SMA and COL1A1 expression.

Main Results:

  • miR-548c-3p expression was significantly downregulated in rats post-MI.
  • Upregulation of miR-548c-3p improved cardiac function and reduced myocardial fibrosis.
  • miR-548c-3p directly targeted and inhibited the expression of proto-oncogene c-Myb, subsequently reducing fibrosis-related factors α-SMA and COL1A1.

Conclusions:

  • miR-548c-3p plays a protective role against myocardial fibrosis after MI.
  • The mechanism involves targeting c-Myb, thereby inhibiting the expression of fibrosis-related genes.
  • miR-548c-3p represents a potential therapeutic target for mitigating myocardial fibrosis post-MI.

More Related Videos

Histological Quantification of Chronic Myocardial Infarct in Rats09:45

Histological Quantification of Chronic Myocardial Infarct in Rats

Published on: December 11, 2016

15.4K
Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease04:41

Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease

Published on: July 3, 2018

8.6K

Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
24.0K
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.9K
Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
743
Cystic Fibrosis: Management01:24

Cystic Fibrosis: Management

Cystic fibrosis (CF) is an autosomal recessive disorder that predominantly affects individuals of Northern European descent, occurring at a rate of 1 in 3500. It is caused by a genetic mutation in a gene on chromosome 7, most commonly the ΔF508 mutation, that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This results in thicker mucus secretions and obstruction pathologies in multiple organs, including the lungs and sinuses.
Sinus disease and chronic...
485
The Role of Culture01:23

The Role of Culture

Culture plays a crucial role in shaping self-identity and influencing thought and behavior, a foundational interest within social psychology. The multicultural perspective recognizes that individuals do not exist in a vacuum; instead, their experiences, perceptions, and actions are deeply influenced by the intersecting dimensions of their cultural, ethnic, and social group affiliations.Cultural Influence on Self-Identity and Social PerceptionCultural frameworks inform how individuals define...
367
Role of Septins01:02

Role of Septins

Septins are the recently discovered fourth major protein component of the cytoskeleton, along with microfilaments, microtubules, and intermediate filaments. These proteins can associate with other cytoskeletal filaments and carry out varied roles or can be free-floating in the cytoplasm.
Cellular Functions of Septins
Recent studies have revealed the multifaceted roles of septins in various cellular processes such as cytokinesis, ciliogenesis, and neurogenesis. Septins act as scaffolds and...
2.1K