In:
Journal of Cellular and Molecular Medicine, Wiley, Vol. 20, No. 5 ( 2016-05), p. 874-890
Abstract:
Pituitary adenylate cyclase‐activating polypeptide ( PACAP ) is a structurally endogenous peptide with many biological roles. However, little is known about its presence or effects in human adipose‐derived stem cells ( hADSC s). In this study, the expression of PACAP type I receptor ( PAC 1R) was first confirmed in hADSC s. Maxadilan, a specific agonist of PAC 1R, could increase hADSC proliferation as determined by Cell Counting Kit‐8 and cell cycle analysis and promote migration as shown in wound‐healing assays. Maxadilan also showed anti‐apoptotic activity in hADSC s against serum withdrawal‐induced apoptosis based on Annexin V/propidium iodide analysis and mitochondrial membrane potential assays. The anti‐apoptotic effects of maxadilan correlated with the down‐regulation of Cleaved Caspase 3 and Caspase 9 as well as up‐regulation of Bcl‐2. The chemical neural differentiation potential could be enhanced by maxadilan as indicated through quantitative PCR , Western blot and cell morphology analysis. Moreover, cytokine neural redifferentiation of hADSC s treated with maxadilan acquired stronger neuron‐like functions with higher voltage‐dependent tetrodotoxin‐sensitive sodium currents, higher outward potassium currents and partial electrical impulses as determined using whole‐cell patch clamp recordings. Maxadilan up‐regulated the Wnt/β‐catenin signalling pathway associated with dimer‐dependent activity of PAC 1R, promoting cell viability that was inhibited by XAV 939, and it also activated the protein kinase A ( PKA ) signalling pathway associated with ligand‐dependent activity of PAC 1R, enhancing cell viability and neural differentiation potential that was inhibited by H‐89. In summary, these results demonstrated that PAC 1R is present in hADSC s, and maxadilan could enhance hADSC viability and neural differentiation potential in neural differentiation medium.
Type of Medium:
Online Resource
ISSN:
1582-1838
,
1582-4934
DOI:
10.1111/jcmm.2016.20.issue-5
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
2076114-4
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