TY - GEN
T1 - PKGIα inhibits the proliferation of cerebral arterial smooth muscle cell induced by oxyhemoglobin after subarachnoid hemorrhage
AU - Luo, Chunxia
AU - Yi, Bin
AU - Chen, Zhi
AU - Tang, Weihua
AU - Chen, Yujie
AU - Hu, Rong
AU - Liu, Zhi
AU - Feng, Hua
AU - Zhang, John H.
N1 - Funding Information:
This research job is supported by Grant No. 30700347, 30500662, 30772224 and 30801186 from the National Science Foundation of China (NSFC) and Grant No.2007BB5045 from the Natural Science Foundation of Chongqing, China.
PY - 2011
Y1 - 2011
N2 - The purpose of the present study was to observe the proliferation of cerebral arterial smooth muscle cell (CASMC) induced by oxyhemoglobin (Oxyhb) and interfered by Adenovirus-mediate-PKGI (Ad-PKGI), and to investigate the potential regulative role of the PKGI gene in the molecule mechanism of cerebral vasospasm (CVS) after Subarachnoid hemorrhage (SAH). Tissue-sticking method was used for primary cultured rat CASMCs. Semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and western blot were used to examine the PKGI mRNA and protein expressions after CASMC were transfected by Ad-PKG. The proliferation of CASMCs was determined by MTT assay and 3H-TdR incorporation. Ad-PKGI could be transfected into CASMCS and highly express. Oxyhemoglobin could stimulate the proliferation of CASMC; the value of 3H-TdR incorporation and the absorbance value of MTT increased and could block up after CASMC was transfected by Ad-PKG. The results suggested that the PKG signaling pathway might play an important role in CVS after SAH, and the PKG gene might be a target point of gene therapy.
AB - The purpose of the present study was to observe the proliferation of cerebral arterial smooth muscle cell (CASMC) induced by oxyhemoglobin (Oxyhb) and interfered by Adenovirus-mediate-PKGI (Ad-PKGI), and to investigate the potential regulative role of the PKGI gene in the molecule mechanism of cerebral vasospasm (CVS) after Subarachnoid hemorrhage (SAH). Tissue-sticking method was used for primary cultured rat CASMCs. Semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and western blot were used to examine the PKGI mRNA and protein expressions after CASMC were transfected by Ad-PKG. The proliferation of CASMCs was determined by MTT assay and 3H-TdR incorporation. Ad-PKGI could be transfected into CASMCS and highly express. Oxyhemoglobin could stimulate the proliferation of CASMC; the value of 3H-TdR incorporation and the absorbance value of MTT increased and could block up after CASMC was transfected by Ad-PKG. The results suggested that the PKG signaling pathway might play an important role in CVS after SAH, and the PKG gene might be a target point of gene therapy.
KW - Cerebral arterial smooth muscle cells (CAMSCs)
KW - Cerebral vasospasm (CVS)
KW - Oxyhemoglobin (Oxyhb)
KW - Protein kinase G (PKG)
KW - Subarachnoid hemorrhage (SAH)
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U2 - 10.1007/978-3-7091-0353-1_29
DO - 10.1007/978-3-7091-0353-1_29
M3 - Conference contribution
C2 - 21116934
SN - 9783709103524
T3 - Acta Neurochirurgica, Supplementum
SP - 167
EP - 171
BT - Early Brain Injury or Cerebral Vasospasm
PB - Springer-Verlag Wien
ER -