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Search Results: 1 - 10 of 54522 matches for " Chia-Chao Wu "
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Role of T Cells in Type 2 Diabetic Nephropathy
Chia-Chao Wu,Huey-Kang Sytwu,Kuo-Cheng Lu,Yuh-Feng Lin
Experimental Diabetes Research , 2011, DOI: 10.1155/2011/514738
Abstract: Type 2 diabetic nephropathy (DN) is the most common cause of end-stage renal disease and is increasingly considered as an inflammatory disease characterized by leukocyte infiltration at every stage of renal involvement. Inflammation and activation of the immune system are closely involved in the pathogenesis of diabetes and its microvascular complications. Macrophage has been well recognized to play an important role in type 2 DN, leukocyte infiltration, and participated in process of DN, as was proposed recently. Th1, Th2, Th17, T reg, and cytotoxic T cells are involved in the development and progression of DN. The purpose of this review is to assemble current information concerning the role of T cells in the development and progression of type 2 DN. Specific emphasis is placed on the potential interaction and contribution of the T cells to renal damage. The therapeutic strategies involving T cells in the treatment of type 2 DN are also reviewed. Improving knowledge of the recognition of T cells as significant pathogenic mediators in DN reinforces the possibility of new potential therapeutic targets translated into future clinical treatments.
Role of Vitamin D in Insulin Resistance
Chih-Chien Sung,Min-Tser Liao,Kuo-Cheng Lu,Chia-Chao Wu
Journal of Biomedicine and Biotechnology , 2012, DOI: 10.1155/2012/634195
Abstract: Vitamin D is characterized as a regulator of homeostasis of bone and mineral metabolism, but it can also provide nonskeletal actions because vitamin D receptors have been found in various tissues including the brain, prostate, breast, colon, pancreas, and immune cells. Bone metabolism, modulation of the immune response, and regulation of cell proliferation and differentiation are all biological functions of vitamin D. Vitamin D may play an important role in modifying the risk of cardiometabolic outcomes, including diabetes mellitus (DM), hypertension, and cardiovascular disease. The incidence of type 2 DM is increasing worldwide and results from a lack of insulin or inadequate insulin secretion following increases in insulin resistance. Therefore, it has been proposed that vitamin D deficiency plays an important role in insulin resistance resulting in diabetes. The potential role of vitamin D deficiency in insulin resistance has been proposed to be associated with inherited gene polymorphisms including vitamin D-binding protein, vitamin D receptor, and vitamin D 1alpha-hydroxylase gene. Other roles have been proposed to involve immunoregulatory function by activating innate and adaptive immunity and cytokine release, activating inflammation by upregulation of nuclear factor κB and inducing tumor necrosis factor α, and other molecular actions to maintain glucose homeostasis and mediate insulin sensitivity by a low calcium status, obesity, or by elevating serum levels of parathyroid hormone. These effects of vitamin D deficiency, either acting in concert or alone, all serve to increase insulin resistance. Although there is evidence to support a relationship between vitamin D status and insulin resistance, the underlying mechanism requires further exploration. The purpose of this paper was to review the current information available concerning the role of vitamin D in insulin resistance.
Role of T Cells in Type 2 Diabetic Nephropathy
Chia-Chao Wu,Huey-Kang Sytwu,Kuo-Cheng Lu,Yuh-Feng Lin
Journal of Diabetes Research , 2011, DOI: 10.1155/2011/514738
Abstract: Type 2 diabetic nephropathy (DN) is the most common cause of end-stage renal disease and is increasingly considered as an inflammatory disease characterized by leukocyte infiltration at every stage of renal involvement. Inflammation and activation of the immune system are closely involved in the pathogenesis of diabetes and its microvascular complications. Macrophage has been well recognized to play an important role in type 2 DN, leukocyte infiltration, and participated in process of DN, as was proposed recently. Th1, Th2, Th17, T reg, and cytotoxic T cells are involved in the development and progression of DN. The purpose of this review is to assemble current information concerning the role of T cells in the development and progression of type 2 DN. Specific emphasis is placed on the potential interaction and contribution of the T cells to renal damage. The therapeutic strategies involving T cells in the treatment of type 2 DN are also reviewed. Improving knowledge of the recognition of T cells as significant pathogenic mediators in DN reinforces the possibility of new potential therapeutic targets translated into future clinical treatments. 1. Introduction Diabetes mellitus (DM) is a complex syndrome characterized by absolute or relative insulin deficiency leading to hyperglycemia and an altered metabolism of glucose, fat, and protein. These metabolic dysfunctions are pathologically associated with specific microvascular diseases and various characteristic long-term complications, including diabetic neuropathy, nephropathy, and retinopathy. Diabetic nephropathy (DN), affecting more than one third of patients with type 1 DM and up to 25% of all patients with type 2 DM, is an extremely common complication of DM that profoundly contributes to patient morbidity and mortality [1–4]. Diabetic nephropathy is a leading cause of chronic kidney disease, resulting in end-stage renal disease (ESRD) which has became a major problem facing human health worldwide [1–4]. Rapidly increasing rates of DM with profound consequences of DN are the primary reason for this worldwide increase. Diabetic nephropathy (DN) is characterized as pathological findings of hypertrophy of glomerular structures, thickening of the basement membrane, and accumulation of extracellular matrix (ECM) components. Multiple mechanisms contribute to the development and outcomes of DN, such as an interaction between metabolic abnormalities, hemodynamic changes, genetic predisposition and inflammatory milieu, and oxidative stress, constituting a continuous perpetuation of injury factors for the
Biomarkers in Acute Kidney Injury  [PDF]
Cai-Mei Zheng, Min-Tser Liao, Mei-Yu Lin, Lan Lo, Chia-Chao Wu, Yung-Ho Hsu, Yuh-Feng Lin, Kuo-Cheng Lu
Open Journal of Nephrology (OJNeph) , 2013, DOI: 10.4236/ojneph.2013.31009
Abstract: Acute kidney injury (AKI) is one of the popular topics of discussions due to increasing development of biomarkers recently. The disease progression and prognosis may be determined by these biomarkers detected in blood and urine specimens. Since acute kidney injury is associated with a broad spectrum of disease conditions, prevention and early detection of AKI becomes very important in those clinical settings. Early measurements of AKI biomarkers predict subsequent development of intrinsic AKI, dialysis requirement, duration of intensive care unit stay and finally affect mortality. We, here, discuss the acute kidney injury in different clinical situations and associated natures of biomarkers, which may help us guide to prevent and treat AKI more effectively.
Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification
Cai-Mei Zheng,Kuo-Cheng Lu,Chia-Chao Wu,Yung-Ho Hsu,Yuh-Feng Lin
International Journal of Nephrology , 2011, DOI: 10.4061/2011/939613
Abstract: Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications. 1. Introduction Vascular calcification is a kind of extraosseous calcification and is associated with aging physiologically, and a number of disorders including ESRD, diabetes mellitus, and cardiovascular disease pathologically. Multifactorial processes contribute to VC in which derangements in calcium and phosphorus homeostasis plays an important role and becomes popular therapeutic target nowadays. In ESRD patients with vascular calcification, a mixture of intimal and medial calcification has been observed in the effected vessels with dominant medial involvement. The risk of CVD mortality in ESRD patients with vascular calcification is 20 to 30 times higher than that of the general population [1–5]. Although phosphate is important for diverse cellular and physiological functions, impaired renal function with resultant phosphate accumulation with consequent bone and mineral disorders and vascular calcification are major problems among nephrologists. The increased risk of CVD mortality by hyperphosphatemia was partially explained by the predisposition of this population to vascular calcification [6–8]. (Figure 1) Even in early stage CKD, serum phosphorus level disturbances are proved to promote vascular calcification, hypertension, myocardial hypertrophy, and heart failure [9–11]. Current understanding of relationship between phosphorus and those disorders becomes popular in medical field, with the hope of halting or retarding the vascular calcification from the very early status in those patients. Figure 1: Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO 4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals.
Involvement of F-Actin in Chaperonin-Containing t-Complex 1 Beta Regulating Mouse Mesangial Cell Functions in a Glucose-Induction Cell Model
Jin-Shuen Chen,Li-Chien Chang,Chia-Chao Wu,Lai-King Yeung,Yuh-Feng Lin
Experimental Diabetes Research , 2011, DOI: 10.1155/2011/565647
Abstract: The aim of this study is to investigate the role of chaperonin-containing t-complex polypeptide 1 beta (CCT2) in the regulation of mouse mesangial cell (mMC) contraction, proliferation, and migration with filamentous/globular-(F/G-) actin ratio under high glucose induction. A low CCT2 mMC model induced by treatment of small interference RNA was established. Groups with and without low CCT2 induction examined in normal and high (H) glucose conditions revealed the following major results: (1) low CCT2 or H glucose showed the ability to attenuate F/G-actin ratio; (2) groups with low F/G-actin ratio all showed less cell contraction; (3) suppression of CCT2 may reduce the proliferation and migration which were originally induced by H glucose. In conclusion, CCT2 can be used as a specific regulator for mMC contraction, proliferation, and migration affected by glucose, which mechanism may involve the alteration of F-actin, particularly for cell contraction.
Involvement of F-Actin in Chaperonin-Containing t-Complex 1 Beta Regulating Mouse Mesangial Cell Functions in a Glucose-Induction Cell Model
Jin-Shuen Chen,Li-Chien Chang,Chia-Chao Wu,Lai-King Yeung,Yuh-Feng Lin
Journal of Diabetes Research , 2011, DOI: 10.1155/2011/565647
Abstract: The aim of this study is to investigate the role of chaperonin-containing t-complex polypeptide 1 beta (CCT2) in the regulation of mouse mesangial cell (mMC) contraction, proliferation, and migration with filamentous/globular-(F/G-) actin ratio under high glucose induction. A low CCT2?mMC model induced by treatment of small interference RNA was established. Groups with and without low CCT2 induction examined in normal and high (H) glucose conditions revealed the following major results: (1) low CCT2 or H glucose showed the ability to attenuate F/G-actin ratio; (2) groups with low F/G-actin ratio all showed less cell contraction; (3) suppression of CCT2 may reduce the proliferation and migration which were originally induced by H glucose. In conclusion, CCT2 can be used as a specific regulator for mMC contraction, proliferation, and migration affected by glucose, which mechanism may involve the alteration of F-actin, particularly for cell contraction. 1. Introduction Functions of mesangial cell contraction, migration, and proliferation have been reported to be correlated with the development of diabetic nephropathy (DN). Mesangial cell contraction regulating intraglomerular pressure contributes to the occurrence of glomerular hyperfiltration in early DN and then progresses to end-stage renal disease (ESRD) [1]. Alteration in mesangial cell migration may limit repair following mesangiolysis and thereby contribute to the loss of kidney function in diabetic nephropathy [2, 3]. Aberrant proliferation of mesangial cells is commonly observed in DN that can lead to ESRD [4]. As the integrity of cytoskeletons is changed during mesangial cell contraction, migration, and proliferation, actin, the most important cytoskeletal protein, should play a role in the development of DN [5]. Actin is often the most abundant protein in a cell, comprising up to 15% of total protein. The function of actin in eukaryotic cells is ubiquitous, including regulation of cell contraction, adherence, movement, and phagocytosis. Actin in cells is generally present interchangeably between a monomer and a polymer, in which globular-(G-) actin subunits assemble into long filamentous polymers called F-actin. Some cellular functions involving cytoskeletons are regulated by this process of actin polymerization [6]. The chaperonin family may play an important role in maintaining the normal function of actin as the function of chaperone-assisted protein folding in cell allows many cytosolic proteins to attain the correct folded states and functional conformations during protein synthesis or
Ferulic Acid, an Angelica sinensis-Derived Polyphenol, Slows the Progression of Membranous Nephropathy in a Mouse Model
Chao-Wen Cheng,Wen-Liang Chang,Li-Cheng Chang,Chia-Chao Wu,Yuh-Feng Lin,Jin-Shuen Chen
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/161235
Abstract: Membranous nephropathy (MN) is a leading cause of adult nephrotic syndrome but lacks adequate treatment. Different extracts of Angelica sinensis (AS) and one of its active compounds, ferulic acid (FA), were used to evaluate the therapeutic effects in a MN mouse model. The MN model was grouped into three subgroups: no treatment (N-T), treatment at induction of MN (Pre-T), and treatment after full-blown MN (Post-T). The results showed that the methanol (ME) layer of AS extract exhibited a therapeutic effect on MN-induced proteinuria. The ME layer-enriched compound, FA, improved the hypoalbuminemia, hyperlipidemia, and proteinuria in both Pre-T and Post-T groups. Ferulic acid also reduced the formation of oxidative protein products and increased the synthesis of antioxidant enzymes in groups Pre-T and Post-T. Regarding angiogenesis factors, the antiangiogenic factors in renal glomeruli were increased in group N-T, but, after FA treatment, only one of the antiangiogenic factors, thrombospondin-1, showed a significant decrease. Furthermore, the expression of Th2 predominant showed significant decrease in both Pre-T and Post-T groups when compared to that of N-T group. In summary, FA retarded the progression of MN, and the mechanisms involved the regulation of oxidative stresses, angiogenic and antiangiogenic factors, and attenuation of Th2 response.
Insulin Resistance in Patients with Chronic Kidney Disease
Min-Tser Liao,Chih-Chien Sung,Kuo-Chin Hung,Chia-Chao Wu,Lan Lo,Kuo-Cheng Lu
Journal of Biomedicine and Biotechnology , 2012, DOI: 10.1155/2012/691369
Abstract: Metabolic syndrome and its components are associated with chronic kidney disease (CKD) development. Insulin resistance (IR) plays a central role in the metabolic syndrome and is associated with increased risk for CKD in nondiabetic patients. IR is common in patients with mild-to-moderate stage CKD, even when the glomerular filtration rate is within the normal range. IR, along with oxidative stress and inflammation, also promotes kidney disease. In patients with end stage renal disease, IR is an independent predictor of cardiovascular disease and is linked to protein energy wasting and malnutrition. Systemic inflammation, oxidative stress, elevated serum adipokines and fetuin-A, metabolic acidosis, vitamin D deficiency, depressed serum erythropoietin, endoplasmic reticulum stress, and suppressors of cytokine signaling all cause IR by suppressing insulin receptor-PI3K-Akt pathways in CKD. In addition to adequate renal replacement therapy and correction of uremia-associated factors, thiazolidinedione, ghrelin, protein restriction, and keto-acid supplementation are therapeutic options. Weight control, reduced daily prednisolone dosage, and the use of cyclosporin decrease the risk of developing new-onset diabetes after kidney transplantation. Improved understanding of the pathogenic mechanisms underlying IR in CKD may lead to more effective therapeutic strategies to reduce uremia-associated morbidity and mortality.
Approaching Biomarkers of Membranous Nephropathy from a Murine Model to Human Disease
Chia-Chao Wu,Jin-Shuen Chen,Ching-Feng Huang,Chun-Chi Chen,Kuo-Chen Lu,Pauling Chu,Huey-Kang Sytwu,Yuh-Feng Lin
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/581928
Abstract: Background. Membranous glomerulonephropathy (MN) is the most prevalent cause of nephrotic syndrome in adult humans. However, the specific biomarkers of MN have not been fully elucidated. We examined the alterations in gene expression associated with the development of MN. Methods. Murine MN was induced by cationic bovine serum albumin (cBSA). After full-blown MN, cDNA microarray analysis was performed to identify gene expression changes, and highly expressed genes were evaluated as markers both in mice and human kidney samples. Results. MN mice revealed clinical proteinuria and the characteristic diffuse thickening of the glomerular basement membrane. There were 175 genes with significantly different expressions in the MN kidneys compared with the normal kidneys. Four genes, metallothionein-1 (Mt1), cathepsin D (CtsD), lymphocyte 6 antigen complex (Ly6), and laminin receptor-1 (Lamr1), were chosen and quantified. Mt1 was detected mainly in tubules, Lamr1 was highly expressed in glomeruli, and CtsD was detected both in tubules and glomeruli. The high expressions of Lamr1 and CtsD were also confirmed in human kidney biopsies. Conclusion. The murine MN model resembled the clinical and pathological features of human MN and may provide a tool for investigating MN. Applying cDNA microarray analysis may help to identify biomarkers for human MN.
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