Hypoxia Mesenchymal Stem Cells Accelerate Wound Closure Improvement by Controlling α-smooth Muscle actin Expression in the Full-thickness Animal Model

Nur Fitriani Hamra; Agung Putra; Arya Tjipta; Nur Dina Amalina; Taufiqurrachman Nasihun

doi:10.3889/oamjms.2021.5537

Authors

Nur Fitriani Hamra Postgraduate Student of Biomedical Sciences Department, Medical Faculty, Sultan Agung Islmaic University (UNISSULA), Semarang Central Java, Indonesia
Agung Putra Stem Cell and Cancer Research (SCCR) Medical Faculty, Sultan Agung Islamic University (UNISSULA), Semarang, Central Java, Indonesia; Department of Posgraduate Biomedical Science, Medical Faculty, Sultan Agung Islamic University (UNISSULA), Semarang, Central Java, Indonesia; Department of Pathological Anatomy, Medical Faculty, Sultan Agung Islmaic University (UNISSULA), Semarang, Central Java, Indonesia http://orcid.org/0000-0003-4261-9437
Arya Tjipta Surgery Department, Medical Faculty, Universitas Sumatera Utara, Medan, North Sumatera, Indonesia
Nur Dina Amalina Stem Cell and Cancer Research (SCCR) Medical Faculty, Sultan Agung Islamic University (UNISSULA), Semaran; Pharmacy Study Program, Chemistry Department, Faculty of Mathematics and Natrual Sciences, Universitas Negeri Semarang, Semarang, Central Java, Indonesiag, Central Java, Indonesia
Taufiqurrachman Nasihun Department of Biochemistry, Medical Faculty, Sultan Agung Islamic University (UNISSULA), Semarang, Central Java, Indonesia

DOI:

https://doi.org/10.3889/oamjms.2021.5537

Keywords:

HMSCs, α-SMA, Wound closure, full-thickness wound model

Abstract

BACKGROUND: The active myofibroblast producing extracellular matrix deposition regarding wound closure is characterized by alpha-smooth muscle actin (α-SMA) expression. However, the persistence of α-SMA expression due to prolonged inflammation may trigger scar formation. A new strategy to control α-SMA expression in line with wound closure improvement uses hypoxic mesenchymal stem cells (HMSCs) due to their ability to firmly control inflammation for early initiating cell proliferation, including the regulation of α-SMA expression associated with wound closure acceleration.

AIM: This study aimed to explore the role of HMSCs in accelerating the optimum wound closure percentages through controlling the α-SMA expression.

MATERIALS AND METHODS: Twenty-four full-thickness rats wound model were randomly divided into four groups: Sham (Sh), Control (C) by NaCl administration only, and two treatment groups by HMSCs at doses of 1.5×106 cells (T1) and HMSCs at doses of 3×106 cells (T2). HMSCs were incubated under hypoxic conditions. The α-SMA expression was analyzed under immunohistochemistry staining assay, and the wound closure percentage was analyzed by ImageJ software.

RESULTS: This study showed a significant increase in wound closure percentage in all treatment groups that gradually initiated on days 6 and 9 (p < 0.05). In line with the increase of wound closure percentages on day 9, there was also a significant decrease in α-SMA expression in all treatment groups (p < 0.05), indicating the optimum wound healing has preceded.

CONCLUSION: HMSCs have a robust ability to accelerated wound closure improvement to the optimum wound healing by controlling α-SMA expression depending on wound healing phases.

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