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CTGF-Primed Wharton’s Jelly Mesenchymal Stem Cells Enhance Collagen Expression for Soft Tissue Regeneration

Quan Fu Gan 1 ORCID logo
Li Zhang 2 ORCID logo
Soon Keng Cheong 3 ORCID logo
Kenny Voon 4 ORCID logo
Chye Wah Yu 5
Zhen Yun Siew 4 ORCID logo
Pooi Pooi Leong 1, * ORCID logo
  1. Department of Pre-clinical Sciences, M. Kandiah Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Sungai Long Campus, Selangor, Malaysia
  2. Department of Human Anatomy, School of Basic Medical Sciences, Binzhou Medical University, Yandai, Shandong, China
  3. Department of Medicine, M. Kandiah Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Sungai Long Campus, Selangor, Malaysia
  4. School of Pharmacy, University of Nottingham Malaysia, Jalan Broga, Semenyih, Selangor, Malaysia
  5. Faculty of Allied Health Sciences, AIMST University, Bedong, Kedah, Malaysia
Correspondence to: Pooi Pooi Leong, Department of Pre-clinical Sciences, M. Kandiah Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Sungai Long Campus, Selangor, Malaysia. ORCID: https://orcid.org/0000-0002-0286-6428. Email: leongpp@utar.edu.my.
Volume & Issue: Vol. 12 No. 12 (2025) | Page No.: 8041-8049 | DOI: 10.15419/7qmq4r19
Published: 2025-12-31

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This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. 

Abstract

Background: Connective Tissue Growth Factor (CTGF) is a matricellular protein implicated in modulating mesenchymal stem cell (MSC) behaviour and extracellular matrix remodelling. This study investigated the dose-dependent effects of CTGF, in the presence or absence of Vitamin C, on Wharton’s Jelly-derived MSCs (WJ-MSCs) with respect to morphology, immunophenotype, collagen gene expression, and protein secretion. 

Methods: WJ-MSCs were expanded in vitro and treated with CTGF (0–120 ng/mL) and/or 0.5 mM Vitamin C. Morphological changes were evaluated by light microscopy, while flow cytometry was used to analyze surface marker expression (CD73, CD90, and CD105). Collagen gene expression (Col1a1 and Col3a1) was quantified by RT-qPCR, and protein secretion was measured with ELISA. 

Results: CTGF-treated WJ-MSCs maintained a spindle-shaped morphology and confluent monolayer organization. CD73 expression remained stable at high levels, whereas CD90 and CD105 expression was modulated in a dose-dependent manner. Vitamin C alone downregulated CD105, but this was mitigated by CTGF co-treatment. Col1a1 expression and secretion were significantly increased by CTGF at 50 ng/mL, reaching a maximum at 100 ng/mL with reduced inter-experimental variance. Col3a1 expression was decreased following treatment with CTGF at 10 ng/mL, suggesting a shift in collagen subtype balance. ELISA corroborated increased collagen secretion upon CTGF stimulation. 

Conclusion: CTGF, particularly at 100 ng/mL in combination with Vitamin C, promotes mesenchymal marker expression, stimulates Col1a1 synthesis, and supports an immunoprivileged phenotype in WJ-MSCs. These findings underscore the potential of CTGF for regenerative strategies aimed at extracellular matrix remodelling and targeted cell therapy.

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