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hUC-MSCs Therapy with EVs Booster Improves Recovery in Stage 2 Chronic Kidney Disease with Hypercholesterolemia : a case report Jutadi; Ayu, Dian Respati; Cahyani, Dini; Arda, Adzani Gaisani; Anggoro, Naufal Sebastian
International Journal of Cell and Biomedical Science Vol 3 No 9 (2024)
Publisher : Stem Cell and Cancer Research (SCCR)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.59278/cbs.v3i9.63

Abstract

Hypercholesterolemia is a common metabolic comorbidity that accelerates the progression of chronic kidney disease (CKD). Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) and their secretome, which consist of extracellular vecicles (EVs) and soluble bioactive molecules, have shown potential in modulating inflammation and metabolism. This case report describes significant improvement in serum lipid profile following hUC-MSC and secretome therapy in a patient with stage 2 CKD and hypercholesterolemia. A male patient with CKD stage 2 received two intravenous cycles of hUC-MSC and secretome therapy administered seven months apart. Serial evaluations demonstrated a progressive decline in total cholesterol from 294 mg/dL at baseline to 286 mg/dL after the first treatment and 225 mg/dL after the second. LDL cholesterol decreased from 188 mg/dL to 140 mg/dL, with a mild rebound to 175 mg/dL. HDL cholesterol, initially elevated at 214 mg/dL, showed a modest increase to 220 mg/dL after the first treatment, followed by normalization to 175 mg/dL. Triglyceride levels remained within the normal range (44–51 mg/dL) throughout the observation period. The marked improvement in lipid parameters suggests that hUC-MSC and secretome therapy may exert systemic metabolic regulation via anti-inflammatory, antioxidative, and hepatoprotective mechanisms. hUC-MSC and secretome administration demonstrated potential benefits in lipid homeostasis in a patient with CKD and hypercholesterolemia. These findings support the role of MSC-derived secretome as a promising adjunctive therapeutic approach. Larger controlled trials are warranted to confirm these outcomes and elucidate underlying mechanisms.
Effects of Extracellular pH Modulation on HIF-1α, c-Myc, and FOXO1 Expression in Colorectal Cancer Cells Ibrahim, Sugeng; Putri Rifai, Fauziah Novita; Arda, Adzani Gaisani
International Journal of Cell and Biomedical Science Vol 4 No 10 (2025)
Publisher : Stem Cell and Cancer Research (SCCR)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.59278/cbs.v4i10.67

Abstract

Background: The tumor microenvironment (TME) of colorectal cancer (CRC) is characterized by an inverted pH gradient, with acidic extracellular and alkaline intracellular conditions that promote tumor progression and metabolic reprogramming. This altered pH landscape regulates key transcriptional drivers of glycolysis and proliferation, including hypoxia-inducible factor-1 alpha (HIF-1α), c-Myc, and the tumor suppressor Forkhead Box Protein O1 (FOXO1). Understanding how extracellular pH influences these regulators may provide new insights for pH-targeted cancer therapy. Methods: Human colorectal carcinoma HCT116 cells were cultured for 24 hours under six extracellular pH conditions (5.5–9.2). The expression of HIF-1α, c-Myc, and FOXO1 was quantified using quantitative real-time polymerase chain reaction (qPCR), and relative fold changes were analyzed by the 2^-ΔΔCt method. Results: Acidic conditions (pH 5.5–6.7) markedly upregulated HIF-1α and c-Myc while strongly suppressing FOXO1 expression. Conversely, mild alkalinity (pH 8.4) reversed this pattern, reducing HIF-1α and c-Myc while restoring FOXO1 expression, suggesting a transcriptional shift from glycolytic to oxidative metabolism. At higher alkalinity (pH 9.2), the expression of all three genes declined, indicating a threshold beyond which excessive pH elevation becomes detrimental to cellular regulation. Conclusion: Extracellular pH critically modulates metabolic gene expression in CRC cells. Acidic conditions activate glycolytic and oncogenic pathways via HIF-1α and c-Myc, while mild alkalinity suppresses these signals and reinstates tumor-suppressive FOXO1 activity. Controlled alkalinization of the TME may therefore represent a promising adjunctive approach to disrupt tumor metabolism and limit cancer progression.