A Role of Canonical Transient Receptor Potential 5 Channel in Neuronal Differentiation from A2B5 Neural Progenitor Cells

Store-operated Ca2+ entry (SOCE) channels are the main pathway of Ca2+ entry in non-excitable cells such as neural progenitor cells (NPCs). However, the role of SOCE channels has not been defined in the neuronal differentiation from NPCs. Here, we show that canonical transient receptor potential channel (TRPC) as SOCE channel influences the induction of the neuronal differentiation of A2B5+ NPCs isolated from postnatal-12-day rat cerebrums. The amplitudes of SOCE were significantly higher in neural cells differentiated from proliferating A2B5+ NPCs and applications of SOCE blockers, 2-aminoethoxy-diphenylborane (2-APB), and ruthenium red (RR), inhibited their rise of SOCE. Among TRPC subtypes (TRPC1-7), marked expression of TRPC5 and TRPC6 with turned-off TRPC1 expression was observed in neuronal cells differentiated from proliferating A2B5+ NPCs. TRPC5 small interfering RNA (siRNA) blocked the neuronal differentiation from A2B5+ NPCs and reduced the rise of SOCE. In contrast, TRPC6 siRNA had no significant effect on the neuronal differentiation from A2B5+ NPCs. These results indicate that calcium regulation by TRPC5 would play a key role as a switch between proliferation and neuronal differentiation from NPCs

Genetic Profiling in Human Adipose Tissue-Derived Mesenchymal Stromal Cells from the Idiopathic and Familial Parkin-Deficient Patients of Parkinson`s Disease in Comparison with non-PD patients

Purpose: With an approach of carrying out a transcriptome microarray analysis using early-passage adipose tissue-derived mesenchymal stromal cells from human adult patients with early-onset hereditary parkin deficient Parkinson`s disease (PD) as well as late-onset idiopathic PD, we aimed to understand brain pathology in PD patients. Methods: Here, we isolated human adipose tissue-derived mesenchymal stromal cells (hAD-MSCs) of patients with idiopathic PD and parkin deficient PD in comparison with non-PD patients and profiled their gene expression using Affymetrix cDNA microarray analysis. Human adipose tissue is a rich source of MSCs, providing an abundant and accessible source of adult stem cells. Results: The hAD-MSCs of patients with idiopathic PD were named as "PD", with parkin deficient PD as "Parkin" and with pituitary adenoma as "non-PD" shortly. Initially, Differentially Expressed Genes (DEGs, total 413 genes) were classified and summarized among non-PD, PD and Parkin. Moreover, using K-mean clustering analysis, we grouped DEGs into 7 clusters and gene names and genebank accession numbers between 2 and 6 were arranged. Additionally, the functional groups of human biomarker candidates were organized and compared between non-PD vs. PD and non-PD vs. Parkin. Finally, PD-related differentially regulated genes by oxidative stress were categorized among non-PD, PD and Parkin. Conclusions: This study showed that knowledge of selective gene expression profile derived from PD patients might potentially lead to better understanding of PD pathology and development of early diagnosis and effective therapy targeted their human biomarkers.Glavan G, 2009, ANAT REC, V292, P1849, DOI 10.1002/ar.21026Lindgren HS, 2009, NEUROPSYCHOPHARMACOL, V34, P2477, DOI 10.1038/npp.2009.74Henchcliffe C, 2008, NAT CLIN PRACT NEURO, V4, P600, DOI 10.1038/ncpneuro0924Hoepken HH, 2008, EXP NEUROL, V212, P307, DOI 10.1016/j.expneurol.2008.04.004Moore DJ, 2008, J NEUROCHEM, V105, P1806, DOI 10.1111/j.1471-4159.2008.05261.xInfante J, 2008, EUR J NEUROL, V15, P431, DOI 10.1111/j.1468-1331.2008.02092.xWada-Isoe K, 2008, J NEUROL SCI, V266, P20, DOI 10.1016/j.jns.2007.08.018MCCOY MK, 2008, J NEUROINFLAMM, V17, P45Goris A, 2007, J NEUROL, V254, P846, DOI 10.1007/s00415-006-0414-6Di Fonzo A, 2007, NEUROLOGY, V68, P1557Morales I, 2007, AM J PHYSIOL-CELL PH, V292, pC1934, DOI 10.1152/ajpcell.00593.2006Dominici M, 2006, CYTOTHERAPY, V8, P315, DOI 10.1080/14653240600855905Abou-Sleiman PM, 2006, NAT REV NEUROSCI, V7, P207, DOI 10.1038/nrn1868Grunblatt E, 2004, J NEURAL TRANSM, V111, P1543, DOI 10.1007/s00702-004-0212-1Yoo MS, 2004, NEUROCHEM RES, V29, P1223Muftuoglu M, 2004, MOVEMENT DISORD, V19, P544, DOI 10.1002/mds.10695Palacino JJ, 2004, J BIOL CHEM, V279, P18614, DOI 10.1074/jbc.M401135200Henry B, 2003, EXP NEUROL, V183, P458, DOI 10.1016/S0014-4886(03)00064-5Zuk PA, 2002, MOL BIOL CELL, V13, P4279, DOI 10.1091/mbc.E02-02-0105Farkas LM, 2002, J NEURAL TRANSM, V109, P267Levite M, 2001, EUR J IMMUNOL, V31, P3504Picklo MJ, 2001, BRAIN RES, V916, P229Soukas A, 2000, GENE DEV, V14, P963Pittenger MF, 1999, SCIENCE, V284, P143Bruder SP, 1998, CLIN ORTHOP RELAT R, pS247DEWITT DA, 1994, BRAIN RES, V656, P205