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Journal : Universa Medicina

Hypoxia enhances self-renewal properties and markers of mesenchymal stem cells Yustianingsih, Vivi; Sumarawati, Titiek; Putra, Agung
Universa Medicina Vol 38, No 3 (2019)
Publisher : Faculty of Medicine, Trisakti University

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (668.593 KB) | DOI: 10.18051/UnivMed.2019.v38.164-171

Abstract

BackgroundMesenchymal stem cells (MSCs) are multipotent stromal cells that express CD73, CD90, and CD105 surface markers, but not CD14, CD45, CD34, CD11b, and HLA-DR. MSCs under hypoxic conditions have the essential role of maintaining the stemness capacity by releasing several growth factors into their medium, known as hypoxia conditioned medium (HCM). This study was performed to compare the effect of percentage of HCM to normoxic medium (NM) in increasing MSC proliferation marked by proliferation rate and surface marker expression.MethodsThis study was of post-test only control group design using human umbilical cord-MSCs (hUC-MSCs) as subjects. The HCM treatment group was obtained by culturing MSCs under 5% O2, whereas the NM control group was grown under 20% O2. The hUC-MSCs were divided into 4 groups with different dose ratios of HCM to NM (25%:75%; 50%:50%; 75%:25% for P1, P2 and P3, respectively and 100% of NM for the controls). All of these groups were maintained at 37oC and the data was collected after 72 hours incubation. MSC marker expression of CD73, CD90 and CD105 was analyzed using flow cytometry and MSC proliferation by trypan blue assay. ResultThere were significant differences in MSC marker expression of CD73, CD90 and CD105 and proliferation at all dose ratios of HCM to NM (p<0.05).ConclusionLow oxygen concentration promotes MSC proliferation and stemness thus it might be beneficial for maintaining the MSC physiologic niche in-vitro.
Hypoxia-preconditioned mesenchymal stem cells attenuate proinflammatory cytokines in collagen loss animal model Fristiani, Yeni; Putra, Agung; Sumarawati, Titiek; Setiawan, Eko; Ibrahim, Sugeng; Pramukarso, Dodik Tugasworo Pramukarso
Universa Medicina Vol. 44 No. 2 (2025)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2025.v44.131-140

Abstract

Background Repeated ultraviolet-B (UVB) exposure induces significant collagen degradation, primarily through overproduction of reactive oxygen species, which subsequently drives an inflammatory cascade. Hypoxia-preconditioned mesenchymal stem cells (H-MSCs) constitute a promising therapeutic approach to counteract collagen loss by modulating inflammatory pathways. This study aimed to evaluate the potential of H-MSCs in regulating NF-κB p65 and IL-1β expression in a collagen loss rat model, highlighting their therapeutic efficacy. Methods Twenty-five healthy male Wistar rats were randomly assigned to five groups: K1 (healthy controls), K2 (collagen loss), K3 (collagen loss + hyaluronic acid), K4 (collagen loss + 2.5 × 10⁵ H-MSCs), and K5 (collagen loss + 5 × 10⁵ H-MSCs). Collagen loss was induced by UVB radiation (peak wavelength: 302 nm) for 2 weeks. mRNA expression of NF-κB p65 was quantified by qRT-PCR, while IL-1β levels were assessed using ELISA. The rats were maintained for 14 days before being sacrificed, to allow the H-MSCs to exert their therapeutic effects. Data analysis was by One-way ANOVA with Tukey’s post-hoc test. Results The administration of H-MSCs significantly reduced IL-1β levels in groups K4 (633.14±63.76 pg/mL) and K5 (520.80±123.82 pg/mL) compared to group K2 (931.93±205.80 pg/mL) (p<0.05), with group K5 showing the most substantial reduction. Moreover, H-MSC injection in groups K4 and K5 effectively reduced NF-κB p65 expression levels (1.13±0.50 a.u. and 0.72±0.22 a.u., respectively), compared to group K2 (2.47±0.50 a.u.) (p<0.05), with group K5 providing optimum inhibition. Conclusion This study demonstrated that H-MSCs effectively attenuate UVB-induced inflammation and modulate key inflammatory pathways.