http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
마성권,주수연,김창성,최준석,배은희,이종은,김수완 전남대학교 의과학연구소 2013 전남의대학술지 Vol.49 No.3
The present study aimed to investigate changes in the mammalian target of rapamycin (mTOR) signaling pathway in the obstructed kidney of rats with unilateral ureteral obstruction (UUO). Male Sprague-Dawley rats were unilaterally obstructed by ligation of the left proximal ureter for 7 days. Control rats were treated in the same way except that no ligature was made. The expression levels of phosphorylated phosphatidylinositol 3-kinase (PI3K), Akt, and mTOR were determined in the kidney by semiquantitative immunoblotting. The protein expression levels of transforming growth factor (TGF)-β1,Bax, and Bcl-2 were also determined in the kidney. The phosphorylation of PI3K, Akt,and mTOR was increased in the kidney of ureteral obstruction rats compared with the control. In the obstructed kidney, the protein expression of TGF-β1 and Bax was also increased, whereas Bcl-2 expression was decreased. In conclusion, the phosphorylation of PI3K/Akt/mTOR was increased in the obstructed kidney of rats with UUO.
마성권 대한내과학회 2015 The Korean Journal of Internal Medicine Vol.30 No.3
In conclusion, an integrated analysis of combined biomarkers may enhance their predictive value for diagnosis and prognosis. Prospective well-designed studies of larger populations are needed to establish the usefulness of NGAL as a biomarker for kidney disease.
Activation of the Renal PI3K/Akt/mTOR Signaling Pathway in a DOCA-Salt Model of Hypertension
마성권,최준석,주수연,김하연,김창성,배은희,이종은,김수완 전남대학교 의과학연구소 2012 전남의대학술지 Vol.48 No.3
The present study investigated the changes that occurred in the mammalian target of rapamycin (mTOR) signaling pathway in the kidney as a result of deoxycorticosterone acetate (DOCA)-salt hypertension. Rats were implanted with DOCA strips (200mg/kg) 1 week after unilateral nephrectomy and were then supplied with 0.9% saline to drink. Four weeks after DOCA implantation, systolic blood pressure (SBP) was measured by use of the tail-cuff method. The expression levels of phosphorylated phosphatidylinositol-3-kinase (PI3K), Akt, and mTOR, as well as the protein expression levels of ED-1 and cyclooxygenase-2 (COX-2), transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (SMA), caspase-3, Bax, and Bcl-2, were then examined in the kidney by semiquantitative immunoblotting. DOCA-salt hypertensive rats were found to have significantly increased SBP as well as an increased kidney weight-to-body weight ratio. Moreover, the phosphorylation of PI3K, Akt, and mTOR was increased in the kidney of DOCA-salt hypertensive rats compared with the control, as was the protein expression of ED-1, COX-2, TGF-β1, and α-SMA. The expression levels of caspase-3 and Bax were increased significantly, whereas Bcl-2 expression was decreased. In conclusion,the phosphorylation of PI3K/Akt/mTOR was increased in the kidney of DOCA-salt hypertensive rats.
신혈관성 고혈압 흰쥐 신장에서 Na, K-ATPase 단백 발현 감소
마성권 ( Seong Kwon Ma ),오윤화 ( Yoon Wha Oh ),김인진 ( In Jin Kim ),배은희 ( Eun Hui Bae ),이종은 ( Jong Un Lee ),김수완 ( Soo Wan Kim ) 대한내과학회 2010 대한내과학회지 Vol.78 No.4
목적: 본 연구는 two kidney, one clip (2K1C) 신혈관성 고혈압을 유발한 흰쥐에서 신장의 Na,K-ATPase, 레닌-안지오텐신-알도스테론계(renin-angiotensin-aldosterone system, RAAS) 및 심방나트륨이뇨호르몬(atrial natriuretic peptide, ANP)계가 고혈압 및 신장 손상의 병태생리에 관련되어 있는지를 조사하고자 하였다. 방법: 실험재료는 Sprague-Dawley 숫쥐를 사용하였다. 2K1C 고혈압을 유발하기 위하여 ketamine (50 mg/kg, i.p.) 마취 후 왼쪽 신동맥에 0.25mm 내경의 silver clip을 끼웠다. 4주일 후에 tail-cuff 방법을 이용하여 수축기 혈압을 측정하였으며, 마취하지 않은 상태에서 단두하여 신장을 적출하였다. 신장 조직에서 Na,K-ATPase α1 subunit 단백 발현을 Western blot 분석법에 의하여 조사하였다. 또한, renin, angiotensin-converting enzyme (ACE), aldosterone synthase (CYP11B2), ineralocorticoid receptor (MR) 및 ANP계의 mRNA 발현을 real-time polymerase chain reaction으로 조사하였다. 결과: 실험군에서 수축기 혈압이 유의하게 증가하였으며, 혈장 레닌 활성도 및 혈청 알도스테론 농도가 증가하였다. 또한, 소변량 및 나트륨 분획 배설이 유의하게 증가하였다. Na,K-ATPase α1 subunit의 단백 발현은 클립 신장에서 대조군에 비하여 유의하게 감소하였고, 클립을 끼우지 않은 실험군의 반대쪽 신장의 단백 발현이 클립 신장에 비하여 증가하였다. 신장 조직의 renin, ACE1, CYP11B2 및 MR의 mRNA 발현은 실험군의 클립 신장에서 대조군에 비하여 증가하였고, 클립을 끼우지 않은 반대쪽 신장에서는 클립 신장에 비하여 유의하게 감소하였다. ACE2 mRNA 발현은 대조군, 실험군의 클립 신장 및 반대쪽 신장 모두에서 유의한 차이가 없었다. 또한, 클립 신장 및 반대쪽 신장의 ANP mRNA 발현이 대조군에 비하여 유의하게 증가하였다. 결론: 신혈관성 고혈압 유발 흰쥐에서 전신 및 신장의 국소 RAAS의 활성 증가가 고혈압 및 세뇨관 손상에 기여할 것으로 사료되며, 신장 ANP계의 활성증가는 고혈압에 대한 보상기전으로 작용할 것으로 보인다. 또한, 세뇨관 손상과 관련된 클립 신장의 Na,K-ATPase 발현 감소가 다뇨 및 나트륨 재흡수 장애에 관여할 것으로 생각된다. Background/Aims: This study investigated the role of Na,K-ATPase, the local renin-angiotensin-aldosterone system (RAAS), and atrial natriuretic peptide (ANP) system in the pathogenesis of renal tubular dysfunction and hypertension in rats with two-kidney, one-clip (2K1C) hypertension. Methods: Adult male Sprague-Dawley rats were made 2K1C hypertensive for 4 weeks. The renal expression of Na,K-ATPase was determined by immunoblotting. The mRNA expression of renin, angiotensin-converting enzyme (ACE), aldosterone synthase (CYP11B2), mineralocorticoid receptor (MR), and the ANP system were determined in the kidney using real-time polymerase chain reaction. Results: The blood pressure was increased in the 2K1C rats, compared with controls. The plasma renin activity and serum aldosterone concentrations were increased, as were the urine output and fractional excretion of sodium. The expression of Na,K-ATPase protein was decreased in the clipped kidney, as compared with the control kidney, while it remained unchanged in the contralateral kidney. The mRNA expression of renin, ACE1, CYP11B2, and MR was increased in the clipped kidney, but unchanged in the non-clipped kidney. The mRNA expression of ACE2 did not differ between the groups. The expression of ANP mRNA was increased in both clipped and non-clipped kidneys, as compared with control kidneys. Conclusions: The enhanced activity of the local RAAS may result in to ischemic tubular injury and the development of hypertension in 2K1C rats. The downregulation of Na,K-ATPase associated with tubular injury in the clipped kidney may account for the impaired tubular sodium reabsorption in 2K1C hypertension. (Korean J Med 78:477-484, 2010)