PubMed Health⌕ Search

Biomedical subjects

Fan-Fan Hou

Publications and source records attributed to Fan-Fan Hou.

6 recordsLinked to original sources
PubMed2006

Advanced glycation end products induce actin rearrangement and subsequent hyperpermeability of endothelial cells.

This study aimed to determine the effects of advanced glycation end products (AGEs) on endothelial cytoskeleton morphology and permeability, and to detect the underlying signaling mechanisms involved in these responses. Cultured endothelial cells (ECs) were exposed to AGE-modified human serum albumin (AGE-HSA), and EC cytoskeletal changes were evaluated by observing fluorescence of F-actin following ligation with labeled antibodies. Endothelial permeability was detected by measuring the flux of TRITC-albumin across the EC monolayers. To explore the signaling pathways behind AGE-induced EC alteration, ECs were treated with either soluble anti-AGE receptor (RAGE) IgG, or the MAPK inhibitors PD98059 and SB203580 before AGE-HSA administration. To further elucidate possible involvement of the ERK and p38 pathways in AGE-induced EC changes, adenovirus-carried recombinant constitutive dominant-negative forms of upstream ERK and p38 kinases, namely MEK1(A) and MKK6b(A), were pre-infected into ECs 24 h prior to AGE-HSA exposure. AGE-HSA induced actin cytoskeleton rearrangement, as well as EC hyperpermeability, in a dose and time-dependent manner. The effects were attenuated in cells pretreated with anti-RAGE IgG, PD98059 or SB203580, respectively. EC pre-infection with MEK1(A) and MKK6b(A) also alleviated the effect of AGEs. Furthermore, adenovirus-mediated administration of activated forms of either MEK1 or MKK6b alone induced rearrangement of F-actin and hyperpermeability. The results indicate that ERK and p38 MAPK play important roles in the mediation of AGE-induced EC barrier dysfunction associated with morphological changes of the F-actin.

Actins↗
PubMed2005

[Mechanism of advanced glycation end products-induced hyperpermeability in endothelial cells].

The purpose of the present study was to investigate the effects of advanced glycation end products (AGEs) modified protein on the permeability of endothelium monolayers and morphological changes of actin cytoskeleton. The roles of receptor for AGEs (RAGE), oxidant stress and the activation of p38 MAPK pathway in this pathological procedure were elucidated. Human umbilical vein endothelial cells (HUVECs)-derived cell line (ECV304) were incubated with AGEs modified human serum albumin (AGE-HSA) in concentrations of 12.5, 25, 50, and 100 microg/ml respectively, for 2, 4, 8, 12 and 24 h. As control, HSA of the same concentration was administered to cells. Then TRITC-albumin was added to evaluate Pa value that reflects the permeability of endothelial monolayer. Furthermore, to visualize the morphological changes of actin cytoskeleton, the treated cells were incubated with rhodamine-phalloidin to stain F-actin. The results showed that the trans-endothelial membrane flux of albumin was significantly increased in a concentration- and time-dependent manner upon the stimulation of AGE-HSA, accompanying with actin reorganization. The blockage of AGE and RAGE binding with anti-RAGE IgG and the pharmacological inhibition of NADPH oxidase or p38 MAP kinase greatly attenuated the AGE-induced hyperpermeability response, respectively. These results indicate that RAGE, NADPH oxidase and p38 MAPK are possibly involved in the mediation of AGEs-induced barrier dysfunction and actin cytoskeleton reorganization in endothelial cells.

Actin Cytoskeleton↗
PubMed2005

[Cardiovascular disease in Chinese chronic renal insufficiency patients-epidemiology survey].

OBJECTIVE: Cardiovascular (CV) disease (CVD) is the single most important cause of death among Chinese dialysis patients, accounting for 51% of overall mortality. The study was performed to investigate the prevalence and the spectrum of CVD in Chinese chronic kidney disease (CKD) patients. METHODS: The multicenter Chinese cohort study examined 1239 CKD patients from 7 main medical centers (distributed in 5 regions of China) who were hospitalized between 2002 and 2003. RESULTS: (1) The most prevalent pathological form of CVD was left ventricular (LV) hypertrophy (LVH), accounting for 58.5% of total patients. The prevalence of coronary artery disease (CAD), congestive heart failure (CHF), and cerebrovascular accidents (CVA) was 16.5%, 27.7% and 5.6%, separately. (2) The cohort with minor renal dysfunction (stage 2-3) had higher prevalence of CAD (5.9%) and CVA (1.0%) compared with general population in the same regions. Up to 41.2% of minor CKD patients were complicated with LVH, and 13.8% of them had clinical evidence of CHF. The prevalence of CAD, LVH and CHF increased as glomerular filtration decline. (3) The prevalence of CAD (20.0%) was much lower and the prevalence of CVA (5.4%) was higher in Chinese dialysis patients than that in American dialysis population. There was significant geographical variations in CAD prevalence, but it was not different between genders. CONCLUSION: The CV risk is significantly increased in patients with CKD. Even minor CKD has a major impact on the CV risk. The prevalence of CAD in Chinese dialysis patients is markedly lower than that in American dialysis population.

Adult↗
PubMed2005

[Improvement of left ventricular hypertrophy by anemic-correcting erythropoietin therapy in chronic renal insufficiency].

OBJECTIVE: Left ventricular hypertrophy (LVH) is an independent predictor of morbidity and mortality in dialysis patients. It remains unclear whether efforts to correct anemia in patients with mild-to-moderate chronic renal insufficiency (CRI) can reverse LVH. This prospective multi-center Chinese cohort study evaluates left ventricular mass index (LVMI) evolution in anemic CRI patients with or without recombinant human erythropoietin (rHuEPO) therapy. METHODS: Six centers enrolled 158 patients with serum creatinine from 147 to 400 micromol/L, and 86 of whom with hemoglobin (Hb) levels < 110 g/L received rHuEPO (Group A). Forty patients with comparable Hb levels (< 110 g/L) but did not receive rHuEPO (Group B) and those with Hb >/= 110 g/L (Group C, n = 32) were served as controls. Echocardiographic studies were performed to evaluate LVMI at baseline and every 3 months during a two-year period. RESULTS: At baseline, the prevalence of LVH was 72.1% in Group A, 72.5% in Group B and 59.4% in Group C. LVMI was inversely correlated with Hb levels (r = -0.70, P < 0.01). There was no difference in age, gender, aetiology of renal failure, blood pressure (BP) and cardiovascular risk factors between the 3 groups. The administration of rHuEPO in Group A significantly increased Hb levels from (93.8 +/- 14.6) g/L to (111.2 +/- 10.3) g/L and decreased LVMI from (142.6 +/- 25.7) g/m(2) to (132.4 +/- 18.5) g/m(2). The prevalence of LVH decreased 16.3% after a partial correction of anemia at 24 months, whereas Hb levels in controls (Group B and Group C) tended to decrease and LVMI significantly increased compared with baseline. The prevalence of LVH was significantly increased in Group B and C after 24 months. The percentage of patients whose serum creatinine level doubled during the follow-up was 3.4% in Group A, 15.0% in Group B and 9.4% in Group C, the difference between Group A and Group B being significant (P < 0.05). In addition, good BP control was obtained without any adverse effects. CONCLUSION: High prevalence of LVH was present in pre-dialysis CRI patients, which is associated with severity of anemia. Early treatment of anemia with rHuEPO can reverse LVH in CRI patients.

Adolescent↗
PubMed2004

[Advanced glycation end products accelerate atherosclerosis via enhancement of oxidative stress].

OBJECTIVE: To investigate the effect of advanced glycation end products (AGE) on atheromatous plaque formation and its possible mechanisms. METHODS: Fifty rabbits were randomly divided into five groups of 10 rabbits: group A, fed with hypercholesterolemic diet and injected intravenously with AGE modified rabbit serum albumin (AGE-RSA); group B, fed with hypercholesterolemic diet and injected with unmodified RSA; group C, fed with hypercholesterolemic diet; group D, fed with normal diet alone: and group E, fed with normal diet and injected with AGE-RSA. Ten weeks after the rabbits were killed. Their aortas were taken out and stained with Sudan red IV. The extent of atheromatous plaques in the aortas en face was evaluated by computer-assisted morphometry and by histologic examination. Photoshop system was used to measure the percentage of atheromatous plaques in the area of tunica intima. The depositions of AGE, malondialdehyde modified low-density lipoprotein (MDA-LDL), oxidized low-density lipoprotein (ox-LDL) and expression of receptor of AGE (RAGE) in aortic tissue were detected by using immunohistological staining. The circulating AGE, blood lipids, serum selenium glutathione peroxydase (SeGSHPx) activity, malonyldialdehyde (MDA), and oxidized LDL (ox-LDL) were detected before the experiment and after the rabbits were killed. RESULTS: (1) The relative plaque area was significantly increased in group A (50% +/- 8%) compared with in group B (21% +/- 7%) and group C (29% +/- 6%). No plaque could be found in animals fed with normal diet (group D) even in those receiving repeated injections of AGE-RSA (group E). Depositions of ox-LDL, MDA-LDL and AGE in atherosclerotic lesions increased and RAGE expression were upregulated in the rabbits fed with hypercholesterolemic diet and injected with AGE-RSA (group A) compared with the other four groups. (2) All hypercholesterolemic rabbits showed comparable serum levels of triglyceride and cholesterol. However, the serum levels of AGE, ox-LDL and MDA were significantly higher and the serum level of SeGSHPx was relatively lower in group A compared with those in the other four groups. (3) The serum level of AGE was directly correlated with the serum ox-LDL (r = 0.459, P < 0.01) or serum MDA concentration (r = 0.423, P < 0.05), and inversely correlated with the serum level of SeGSHPx (r = - 0.448, P < 0.01). A close correlation was found between the serum level of AGE and endothelium RAGE expression (r = 0.384, P < 0.05) and deposition area of AGE (r = 0.468, P < 0.05) in aorta. CONCLUSION: AGE accelerates the atheromatous plaque formation through induction of oxidative stress and upregulation of RAGE.

Animals↗