Adipose tissue-derived stem cells secrete CXCL5 cytokine with neurotrophic effects on cavernous nerve regeneration.
Zhang H., Yang R., Wang Z., Lin G., Lue TF., Lin CS.
Animal Study, published in J Sex Med (2010) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Sex Med (2010)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 21114767
- PMCID
- PMC3176296
- DOI
- 10.1111/j.1743-6109.2010.02128.x
- Citations
- 62
Abstract (original English)
Introduction Previously we reported that paracrine actions likely mediated the therapeutic effects of adipose tissue-derived stem cells (ADSCs) on a rat model of cavernous nerve (CN) injury. Aim To identify potential neurotrophic factors in ADSC's secretion, test the most promising one, and identify the molecular mechanism of its neurotrophic action. Methods Rat major pelvic ganglia (MPG) were cultured in conditioned media of ADSC and penile smooth muscle cells (PSMCs). Cytokine expression in these two media was probed with a cytokine antibody array. CXCL5 cytokine was quantified in these two media by enzyme-linked immunosorbent assay (ELISA). Activation of Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) by CXCL5 was tested in neuroblastoma cell lines BE(2)C and SH-SY5Y as well as in Schwann cell line RT4-D6P2T by Western blot. Involvement of CXCL5 and JAK/STAT in ADSC-conditioned medium's neurotrophic effects was confirmed with anti-CXCL5 antibody and JAK inhibitor AG490, respectively. Main outcome measures Neurotrophic effects of ADSC and PSMC-conditioned media were quantified by measuring neurite length in MPG cultures. Secretion of CXCL5 in these two media was quantified by ELISA. Activation of JAK/STAT by CXCL5 was quantified by densitometry on Western blots for STAT1 and STAT3 phosphorylation. Results MPG neurite length was significantly longer in
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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