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Published on: November 23, 2021
Adipose stem-cell-derived microvesicles ameliorate long-term bladder ischemia-induced bladder underactivity.
Bing-Juin Chiang1, Su-Han Mao1, Tung-Sheng Chen2
1College of Medicine, Fu-Jen Catholic University, No. 510, Zhongzheng Rd., Xinzhuang Dist., New Taipei City, 24205, Taiwan; Department of Urology, Cardinal Tien Hospital, No.362, Zhongzheng Rd., Xindian Dist., New Taipei City, 23148, Taiwan; Department of Life Science, College of Science, National Taiwan Normal University, 162, Section 1, Heping E. Rd., Taipei, 106, Taiwan.
Adipose-derived stem cell-derived microvesicles (ADSC-MVs) effectively treat bladder underactivity caused by long-term ischemia. ADSC-MVs improved bladder function, reduced inflammation, and promoted nerve regeneration more than ADSCs.
Area of Science:
- Regenerative Medicine
- Urology
- Cell Biology
Background:
- Long-term hypoxia/ischemia-induced bladder underactivity mechanisms remain unclear.
- Effective therapeutic strategies for this condition are needed.
Purpose of the Study:
- To determine the mechanisms of bladder underactivity induced by bilateral partial iliac arterial occlusion (BPAO).
- To explore the therapeutic potential of adipose-derived stem cells (ADSCs) and ADSC-derived microvesicles (MVs) for BPAO-induced bladder dysfunction.
Main Methods:
- Rats underwent 4-week BPAO induction, followed by treatment with ADSCs or ADSC-MVs via femoral artery injection.
- Evaluated bladder microcirculation, contractility, nerve activity, histology, and molecular markers (P2X2/P2X3, M2/M3, NGF, collagen-1).
Main Results:
- BPAO significantly impaired bladder microcirculation, contractility, and receptor expression, while increasing inflammation and fibrosis.
- ADSC-derived MVs demonstrated superior efficacy compared to ADSCs in restoring bladder function and reducing pathological markers.
Conclusions:
- ADSC-derived MVs are a promising therapy for long-term BPAO-induced detrusor underactivity.
- ADSC-MVs ameliorate inflammation, enhance purinergic/cholinergic signaling, promote neuronal regeneration, and decrease fibrosis, thereby improving bladder function.
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