Biomedical subjects

Yusuke Suzuki

Publications and source records attributed to Yusuke Suzuki.

77 records · Page 5Linked to original sources

PubMed2002

Angiotensin III activates nuclear transcription factor-kappaB in cultured mesangial cells mainly via AT(2) receptors: studies with AT(1) receptor-knockout mice.

Nuclear factor-kappaB (NF-kappaB) regulates many genes involved in renal pathophysiologic processes. It was previously demonstrated that angiotensin II (AngII) and its amino-terminal degradation product AngIII activate NF-kappaB in mesangial cells. However, which are the Ang receptor subtypes involved in the NF-kappaB pathway and whether these Ang peptides act through the same or different receptors in mesangial cells have not been evaluated. Under the culture conditions used, quiescent rat mesangial cells expressed both AT(1) and AT(2) receptors. To investigate the receptors involved in the NF-kappaB pathway, two different approaches were used, i.e., pharmacologic studies, using specific AT(1) and AT(2) receptor antagonists and agonists, and studies in AT(1) receptor-knockout mice. In cultured rat mesangial cells, both AT(1) and AT(2) receptor antagonists inhibited AngII-induced NF-kappaB DNA binding activity, whereas NF-kappaB activation elicited by AngIII was mainly blocked by the AT(2) receptor antagonist. Similar results were observed for cytosolic IkappaBalpha degradation. An AT(2) receptor agonist also activated NF-kappaB. In AT(1) receptor-knockout murine mesangial cells, AngIII and AngII increased NF-kappaB activity and degraded cytosolic IkappaBalpha; both processes were blocked by the AT(2) receptor antagonist. These data demonstrate that, in mesangial cells, NF-kappaB activation is mediated by AT(1) and AT(2) receptors, suggesting a novel intracellular signaling mechanism for AT(2) receptors in the kidney. Some differences in Ang peptide receptor-mediated responses were also observed. AngII activates NF-kappaB via AT(1) and AT(2) receptors, whereas AngIII acts mainly via AT(2) receptors. These results suggest the potential involvement of the AngIII/AT(2) receptor/NF-kappaB pathway in pathophysiologic processes in the kidney and provide a better understanding of the renin-angiotensin system.

Angiotensin III↗

PubMed2002

[Half-solid enteral nutrient prevents chronic complications of percutaneous endoscopic gastrostomy tube feeding].

An 85-year-old woman was receiving enteral feeding via percutaneous endoscopic gastrostomy (PEG). The patient exhibited symptoms of gastro-esophageal reflux, leakage of nutrient from the PEG insertion point, vomiting, pyrexia, dyspnea when given nutrients and recurrent pneumonia. We therefore gave a half-solid nutrient, which was made by a mixture of agar powder and conventional liquid nutrient Immediately after starting the half-solid nutrient feeding via PEG, the patients no longer exhibited the above symptoms apart from mild pyrexia, which also vanished two weeks later. This case suggested that simply changing the fluidity of nutrients can contribute to a reduction of complications expected to occur in patients on PEG tube feeding.

Aged↗

PubMedDate not supplied

Reactive oxygen species-mediated signaling pathways in angiotensin II-induced MCP-1 expression of proximal tubular cells.

Angiotensin II (AngII) has pleiotropic effects, the most well known of which is the generation of reactive oxygen species (ROS) and chemokines in inflammatory lesions. Monocyte chemoattractant protein-1 (MCP-1) is considered a major chemokine in the pathogenesis of kidney diseases. We examined signaling pathways of AngII-induced MCP-1 expression and the role of ROS in the murine proximal tubular cells (mProx) using various inhibitors. Furthermore, we compared the signaling pathways between mProx and mesangial cells (MC). AngII-induced MCP-1 protein expression in mProx at 6 h was largely blocked by ROS (N-acetylcysteine; 82 +/- 14%), Ras (N-acetyl-S-trans,trans-farnesyl-L-cysteine; 82 +/- 13%), and nuclear factor-kappaB (NF-kappaB) (parthenolide; 89 +/- 7.9%) inhibitors. Both AT1 receptor (AT1R) (Olmesartan; 41 +/- 12%) and the AT2R (PD123319; 24 +/- 11%) antagonists partially blocked the MCP-1 expression. Furthermore, mitogen-activated protein kinase (MAPK) pathways were also implicated in this protein expression, but it is less dependent on ROS/Ras pathways. In MC, protein kinase (calphostin C; 84 +/- 2.8%) and NF-kappaB (89 +/- 1.4%) inhibitors attenuated acute AngII-induced MCP-1 expression stronger than ROS/Ras inhibitors (1.0 +/- 0.9/29 +/- 9.5%). MAPK pathways, especially p38 MAPK, were involved in MC more than in mProx. AT1R (69 +/- 8.6%) and AT2R (57 +/- 21%) antagonists also were blocked. We suggested that, although NF-kappaB activation has a critical role, signaling pathways are different between mProx and MC. ROS-mediated signaling in mProx may have more contribution to AngII-induced inflammatory responses than to those in MC.

Angiotensin II↗

PubMedDate not supplied

Prevention of late complications by half-solid enteral nutrients in percutaneous endoscopic gastrostomy tube feeding.

BACKGROUND: Percutaneous endoscopic gastrostomy feeding is accompanied by unique complications, which are not easily controlled. OBJECTIVE: In an attempt to decrease complications, we used half-solid nutrients for percutaneous endoscopic gastrostomy feeding in an 85-year-old woman. The patient had been receiving enteral nutrients via percutaneous endoscopic gastrostomy, and we examined whether this approach can reduce complications. She presented with regurgitation of enteral nutrients and recurrent respiratory infections. METHODS: Half-solid enteral nutrients, prepared by mixing liquid enteral nutrients with agar powder, were administered via percutaneous endoscopic gastrostomy. RESULTS: Symptoms of gastroesophageal reflux disappeared immediately after the start of half-solid enteral nutrient feeding. CONCLUSION: Gastroesophageal reflux and leakage, two intractable late complications of percutaneous endoscopic gastrostomy tube feeding, can be alleviated by the solidification of enteral nutrients. Since this method allows quick administration of nutrients, it is also expected to help prevent the occurrence of decubitus ulcers and reduce the burden to the caregiver.

Aged↗

PubMedDate not supplied

Microdialysis measurement of acetylcholine in rat hippocampus during severe insulin-induced hypoglycemia.

OBJECTIVE: It has been well acknowledged that hypoglycemia induces cognitive impairment. However, the behavior of hippocampal cholinergic system, which is thought to play a key role in cognition, during hypoglycemia remains to be elucidated. MATERIALS AND METHODS: In this study we conducted a microdialysis using 9 weeks old virgin male Wistar/ST rats to determine the changes of extracelluar acethylcholine and glucose levels in the hippocampus during insulin-induced severe hypoglycemia, and compared the results with those obtained from a microdialysis in the striatum. RESULTS: The extracelluar concentrations of acethylcholine both in the hippocampus and striatum did not change during hypoglycemia. CONCLUSION: The results of the present study may suggest that changes of hippocampal cholinergic release may not be involved in the mechanism of cognitive impairment during hypoglycemia.

Acetylcholine↗