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Article ; Online: Nicotine and methyl vinyl ketone, major components of cigarette smoke extracts, increase protective amyloid-β peptides in cells harboring amyloid-β precursor protein.

Ohshima, Yoichi / Iwata, Kazumi / Ibi, Masakazu / Matsumoto, Misaki / Katsuyama, Masato / Yabe-Nishimura, Chihiro

2018 Volume 43, Issue 4, Page(s) 257–266

Abstract: The increased ratio of longer amyloid-β (Aβ1-42)/shorter amyloid-β (Aβ1-40) peptides, generated from amyloid precursor protein (APP), is known to promote the development of Alzheimer's disease (AD). To investigate the role of smoking in Aβ production, we ...

Abstract	The increased ratio of longer amyloid-β (Aβ1-42)/shorter amyloid-β (Aβ1-40) peptides, generated from amyloid precursor protein (APP), is known to promote the development of Alzheimer's disease (AD). To investigate the role of smoking in Aβ production, we determined the production of Aβ species in the presence of nicotine or methyl vinyl ketone (MVK), major components of cigarette smoke extracts, in Flp-In
MeSH term(s)	Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/prevention & control ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Butanones/isolation & purification ; Butanones/pharmacology ; Cells, Cultured ; Cigarette Smoking/metabolism ; Depression, Chemical ; Humans ; Nicotine/isolation & purification ; Nicotine/pharmacology ; Tobacco Products/analysis
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Butanones ; Nicotine (6M3C89ZY6R) ; 3-buten-2-one (AR7642I1MP) ; Amyloid Precursor Protein Secretases (EC 3.4.-)
Language	English
Publishing date	2018
Publishing country	Japan
Document type	Journal Article
ZDB-ID	770623-6
ISSN	1880-3989 ; 0388-1350
ISSN (online)	1880-3989
ISSN	0388-1350
DOI	10.2131/jts.43.257
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Zs.A 1682: Show issues

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Article ; Online: A 10-year longitudinal study of deep white matter lesions on magnetic resonance imaging.

Tamura, Aiko / Kuriyama, Nagato / Akazawa, Kentaro / Ozaki, Etsuko / Watanabe, Isao / Ohshima, Yoichi / Kondo, Masaki / Takezawa, Nobuo / Takada, Akihiro / Matsumoto, Sanae / Takeda, Kazuo / Yoshii, Kengo / Yamada, Kei / Watanabe, Yoshiyuki / Nakagawa, Masanori / Mizuno, Toshiki

Neuroradiology

2021 Volume 63, Issue 10, Page(s) 1599–1609

Abstract: Purpose: Deep white matter lesions (DWMLs), T2 high-intensity areas in the subcortical white matter on magnetic resonance imaging (MRI), are a clinical phenotype of cerebral small vessel disease. Factors such as age and hypertension have been reported ... ...

Abstract	Purpose: Deep white matter lesions (DWMLs), T2 high-intensity areas in the subcortical white matter on magnetic resonance imaging (MRI), are a clinical phenotype of cerebral small vessel disease. Factors such as age and hypertension have been reported to significantly contribute to the presence and severity of DWMLs in cross-sectional studies. We herein report a 10-year longitudinal study on DWMLs in elderly Japanese subjects to reveal the clinical variables contributing to the progression of DWMLs. Methods: A total of 469 Japanese subjects were invited to participate in the study. Of the participants at baseline, 259 subjects completed the revisit MRI study 10 years later. In those 259 subjects, we evaluated the correlation between the progression of DWMLs and clinical variables, such as the gender, age, and overt vascular risk factors. To clarify the role of hypertension, 200 subjects with grade 1 DWMLs at baseline were categorized into three groups according to their status of hypertension and its treatment. Results: Of the 200 subjects with grade 1 DWMLs, 47 subjects (23.5%) showed progression of DWMLs (progression group). In the progression group, the percentage of subjects with hypertension and the systolic blood pressure values were higher than in the non-progression group. In addition, subjects ≥ 60 years old at baseline tended to show deterioration of DWMLs in the group with hypertension without antihypertensive treatment. Conclusion: The results of this 10-year longitudinal study imply a positive correlation between long-standing hypertension and the progression of DWMLs.
MeSH term(s)	Aged ; Brain ; Cerebral Small Vessel Diseases ; Cross-Sectional Studies ; Humans ; Longitudinal Studies ; Magnetic Resonance Imaging ; Middle Aged ; Risk Factors ; White Matter/diagnostic imaging
Language	English
Publishing date	2021-02-18
Publishing country	Germany
Document type	Journal Article
ZDB-ID	123305-1
ISSN	1432-1920 ; 0028-3940
ISSN (online)	1432-1920
ISSN	0028-3940
DOI	10.1007/s00234-020-02626-2
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Zs.A 658: Show issues

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Article: Mutations in the β-amyloid precursor protein in familial Alzheimer's disease increase Aβ oligomer production in cellular models.

Ohshima, Yoichi / Taguchi, Katsutoshi / Mizuta, Ikuko / Tanaka, Masaki / Tomiyama, Takami / Kametani, Fuyuki / Yabe-Nishimura, Chihiro / Mizuno, Toshiki / Tokuda, Takahiko

Heliyon

2018 Volume 4, Issue 1, Page(s) e00511

Abstract: Soluble oligomers of amyloid-β (Aβ) peptides (AβOs) contribute to neurotoxicity in Alzheimer's disease (AD). However, it currently remains unknown whether an increase in AβOs is the common phenotype in cellular and animal models. Furthermore, it has not ... ...

Abstract	Soluble oligomers of amyloid-β (Aβ) peptides (AβOs) contribute to neurotoxicity in Alzheimer's disease (AD). However, it currently remains unknown whether an increase in AβOs is the common phenotype in cellular and animal models. Furthermore, it has not yet been established whether experimental studies conducted using models overexpressing mutant genes of the amyloid precursor protein (APP) are suitable for investigating the underlying molecular mechanism of AD. We herein employed the Flp-In™ T-REx™-293 (T-REx 293) cellular system transfected with a single copy of wild-type, Swedish-, Dutch-, or London-type
Language	English
Publishing date	2018-02-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2018.e00511
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Article: Mutations in the β-amyloid precursor protein in familial Alzheimer’s disease increase Aβ oligomer production in cellular models

Ohshima, Yoichi / Taguchi, Katsutoshi / Mizuta, Ikuko / Tanaka, Masaki / Tomiyama, Takami / Kametani, Fuyuki / Yabe-Nishimura, Chihiro / Mizuno, Toshiki / Tokuda, Takahiko

Heliyon. 2018 Jan., v. 4, no. 1

2018

Abstract: Soluble oligomers of amyloid-β (Aβ) peptides (AβOs) contribute to neurotoxicity in Alzheimer’s disease (AD). However, it currently remains unknown whether an increase in AβOs is the common phenotype in cellular and animal models. Furthermore, it has not ... ...

Abstract	Soluble oligomers of amyloid-β (Aβ) peptides (AβOs) contribute to neurotoxicity in Alzheimer’s disease (AD). However, it currently remains unknown whether an increase in AβOs is the common phenotype in cellular and animal models. Furthermore, it has not yet been established whether experimental studies conducted using models overexpressing mutant genes of the amyloid precursor protein (APP) are suitable for investigating the underlying molecular mechanism of AD. We herein employed the Flp-In™ T-REx™-293 (T-REx 293) cellular system transfected with a single copy of wild-type, Swedish-, Dutch-, or London-type APP, and quantified the levels of Aβ monomers (Aβ1-40 and Aβ1-42) and AβOs using an enzyme-linked immunosorbent assay (ELISA). The levels of extracellular AβOs were significantly higher in Dutch- and London-type APP-transfected cells than in wild-type APP-transfected cells. Increased levels were also observed in Swedish-type APP-transfected cells. On the other hand, intracellular levels of AβOs were unaltered among wild-type and mutant APP-transfected cells. Intracellular levels of Aβ monomers were undetectable, and no common abnormality was observed in their extracellular levels or ratios (Aβ1-42/Aβ1-40) among the cells examined. We herein demonstrated that increased levels of extracellular AβOs are the common phenotype in cellular models harboring different types of APP mutations. Our results suggest that extracellular AβOs play a key role in the pathogenesis of AD.
Keywords	amyloid ; animals ; enzyme-linked immunosorbent assay ; mutants ; neurotoxicity ; pathogenesis ; peptides ; phenotype
Language	English
Dates of publication	2018-01
Publishing place	Elsevier Ltd
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2018.e00511
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Article ; Online: Clioquinol increases the expression of VGF, a neuropeptide precursor, through induction of c-Fos expression.

Katsuyama, Masato / Ibi, Masakazu / Matsumoto, Misaki / Iwata, Kazumi / Ohshima, Yoichi / Yabe-Nishimura, Chihiro

Journal of pharmacological sciences

2014 Volume 124, Issue 4, Page(s) 427–432

Abstract: Clioquinol was used extensively in the mid-1900s as an amebicide to treat indigestion and diarrhea. It was eventually withdrawn from the market because it was linked to subacute myelo-optic neuropathy (SMON) in Japan. However, the pathogenesis of SMON ... ...

Abstract	Clioquinol was used extensively in the mid-1900s as an amebicide to treat indigestion and diarrhea. It was eventually withdrawn from the market because it was linked to subacute myelo-optic neuropathy (SMON) in Japan. However, the pathogenesis of SMON has not yet been elucidated in detail. As reported previously, we performed a global analysis on human neuroblastoma cells using DNA chips. The global analysis and quantitative PCR demonstrated that the mRNA level of VGF (nonacronymic), the precursor of neuropeptides involved in pain reactions, was significantly increased when SH-SY5Y and IMR-32 neuroblastoma cells were treated with clioquinol. Promoter analyses in SH-SY5Y cells revealed that a region responsive to clioquinol exists between -1381 and -1349 of the human VGF gene, which contains an activator protein (AP)-1 site-like sequence. The introduction of mutations at this site significantly reduced clioquinol-induced transcriptional activation. Clioquinol induced the expression of the AP-1 family transcription factors, c-Jun and c-Fos. Electrophoresis mobility shift assays demonstrated that c-Jun and c-Fos could bind to the AP-1 site at -1374/-1368 in SH-SY5Y cells treated with clioquinol. RNA interference against c-Fos significantly suppressed clioquinol-induced VGF mRNA expression. These results suggest that the clioquinol-induced expression of c-Fos mediates the induction of VGF expression.
MeSH term(s)	Amebicides/adverse effects ; Amebicides/pharmacology ; Clioquinol/adverse effects ; Clioquinol/pharmacology ; Gene Expression/drug effects ; Humans ; Myelitis/chemically induced ; Nerve Growth Factors/genetics ; Nerve Growth Factors/metabolism ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Oligonucleotide Array Sequence Analysis ; Optic Neuritis/chemically induced ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-fos/metabolism ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; RNA Interference/physiology ; RNA, Messenger/metabolism ; Transcription Factor AP-1/genetics ; Transcription Factor AP-1/metabolism ; Tumor Cells, Cultured
Chemical Substances	Amebicides ; Nerve Growth Factors ; Neuropeptides ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; RNA, Messenger ; Transcription Factor AP-1 ; VGF protein, human ; Clioquinol (7BHQ856EJ5)
Language	English
Publishing date	2014-03-19
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1254/jphs.13271fp
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Zs.A 237: Show issues

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Article ; Online: Regulation of axonal elongation and pathfinding from the entorhinal cortex to the dentate gyrus in the hippocampus by the chemokine stromal cell-derived factor 1 alpha.

Ohshima, Yoichi / Kubo, Takekazu / Koyama, Ryuta / Ueno, Masaki / Nakagawa, Masanori / Yamashita, Toshihide

The Journal of neuroscience : the official journal of the Society for Neuroscience

2008 Volume 28, Issue 33, Page(s) 8344–8353

Abstract: During the early developmental stage, a neural circuit is established between the entorhinal cortex (EC) and the hippocampal dentate gyrus (DG) via the perforant pathway. However, the manner in which the perforant fibers are navigated has mostly remained ...

Abstract	During the early developmental stage, a neural circuit is established between the entorhinal cortex (EC) and the hippocampal dentate gyrus (DG) via the perforant pathway. However, the manner in which the perforant fibers are navigated has mostly remained a mystery. Here, we analyzed the functional role of a chemokine, namely, stromal cell-derived factor 1alpha (SDF-1alpha), in the navigation of the perforant fibers. SDF-1alpha was observed to promote neurite growth, which is dependent on mDia1, in cultured entorhinal cortical neurons obtained from rats at postnatal day 0. We then used entorhino-hippocampal cocultures comprising green fluorescence-labeled EC and DG slices to assess the projection of the perforant fibers from the EC. Although the specific laminar termination of the entorhinal axons was observed with this system, the number of appropriately terminating entorhinal axons decreased significantly when the SDF-1alpha signaling pathway was blocked by a neutralizing antibody against SDF-1alpha or by the specific SDF-1alpha receptor antagonist AMD3100 (1,1'-[1,4-phenylenebis(methylene)]bis-1,4,8,11-tetra-azacyclotetradecane octahydrochloride). Furthermore, inhibition of the SDF-1alpha signaling pathway resulted in a decrease in the immunoreactivity for PSD-95 (postsynaptic density protein-95) in the DG, possibly because of a reduction in the number of projecting perforant fibers. These results demonstrate that SDF-1alpha plays a critical role in promoting the growth of perforant fibers from the EC to the DG.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Axons/physiology ; Cells, Cultured ; Chemokine CXCL12/physiology ; Dentate Gyrus/physiology ; Entorhinal Cortex/physiology ; Hippocampus/physiology ; Organ Culture Techniques ; Perforant Pathway/drug effects ; Perforant Pathway/physiology ; Rats
Chemical Substances	Chemokine CXCL12
Language	English
Publishing date	2008-08-13
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1670-08.2008
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Zs.A 1668: Show issues

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Article ; Online: NADPH oxidase NOX1 is involved in activation of protein kinase C and premature senescence in early stage diabetic kidney.

Zhu, Kai / Kakehi, Tomoko / Matsumoto, Misaki / Iwata, Kazumi / Ibi, Masakazu / Ohshima, Yoichi / Zhang, Jia / Liu, Junjie / Wen, Xiaopeng / Taye, Ashraf / Fan, Chunyuan / Katsuyama, Masato / Sharma, Kumar / Yabe-Nishimura, Chihiro

Free radical biology & medicine

2015 Volume 83, Page(s) 21–30

Abstract: Increased oxidative stress and activation of protein kinase C (PKC) under hyperglycemia have been implicated in the development of diabetic nephropathy. Because reactive oxygen species derived from nicotinamide adenine dinucleotide phosphate (NADPH) ... ...

Abstract	Increased oxidative stress and activation of protein kinase C (PKC) under hyperglycemia have been implicated in the development of diabetic nephropathy. Because reactive oxygen species derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, NOX1 accelerate the translocation of PKC isoforms, NOX1 is postulated to play a causative role in the development of diabetic nephropathy. Hyperglycemia was induced in wild-type and Nox1-deficient mice (KO) by two doses of streptozotocin injection. At 3 weeks after the induction of hyperglycemia, glomeruli and cortical tubules were isolated from kidneys. The mRNA level of Nox1 was significantly upregulated in the renal cortex at 3 weeks of hyperglycemia. Urinary albumin and expression of inflammatory or fibrotic mediators were similarly elevated in diabetic wild-type and KO; however, increases in glomerular volume and mesangial matrix area were attenuated in diabetic KO. Nox1 deficiency significantly reduced the levels of renal thiobarbituric acid-reacting substances and 8-hydroxydeoxyguanosine, membranous translocation of PKCα/β, activity of PKC, and phosphorylation of p38 mitogen-activated protein kinase in the diabetic kidney. Furthermore, increased staining of senescence-associated β-galactosidase in glomeruli and cortical tubules of diabetic mice was significantly suppressed in KO. Whereas the levels of cyclin-dependent kinase inhibitors, p16(INK4A) and p21(Cip1), were equivalent between the genotypes, increased levels of p27(Kip1) and γ-H2AX, a biomarker for DNA double-strand breaks, were significantly attenuated in isolated glomeruli and cortical tubules of diabetic KO. Taken together, NOX1 modulates the p38/p27(Kip1) signaling pathway by activating PKC and promotes premature senescence in early stage diabetic nephropathy.
MeSH term(s)	Animals ; Blotting, Western ; Cells, Cultured ; Cellular Senescence/physiology ; Diabetes Mellitus, Experimental/chemically induced ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diabetic Nephropathies/chemically induced ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Glomerular Mesangium/metabolism ; Glomerular Mesangium/pathology ; Hyperglycemia/chemically induced ; Hyperglycemia/metabolism ; Hyperglycemia/pathology ; Immunoenzyme Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NADH, NADPH Oxidoreductases/physiology ; NADPH Oxidase 1 ; Oxidation-Reduction ; Oxidative Stress ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; RNA, Messenger/genetics ; Reactive Oxygen Species/metabolism ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; beta-Galactosidase/metabolism ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	RNA, Messenger ; Reactive Oxygen Species ; NADH, NADPH Oxidoreductases (EC 1.6.-) ; NADPH Oxidase 1 (EC 1.6.3.-) ; NOX1 protein, mouse (EC 1.6.3.-) ; Protein Kinase C (EC 2.7.11.13) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; beta-Galactosidase (EC 3.2.1.23)
Language	English
Publishing date	2015-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2015.02.009
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Zs.A 2109: Show issues

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Article ; Online: Serum albumin to globulin ratio is related to cognitive decline via reflection of homeostasis: a nested case-control study.

BMC neurology

2016 Volume 16, Issue 1, Page(s) 253

Abstract: Background: Recent research suggests that several pathogenetic factors, including aging, genetics, inflammation, dyslipidemia, diabetes, and infectious diseases, influence cognitive decline (CD) risk. However, no definitive candidate causes have been ... ...

Abstract	Background: Recent research suggests that several pathogenetic factors, including aging, genetics, inflammation, dyslipidemia, diabetes, and infectious diseases, influence cognitive decline (CD) risk. However, no definitive candidate causes have been identified. The present study evaluated whether certain serum parameters predict CD. Methods: A total of 151 participants were assessed for CD using the Mini-Mental State Examination (MMSE), and 34 participants were identified as showing CD. Results: Among CD predictive risk factors, Helicobacter pylori seropositivity was significantly predictive of CD risk, more so than classical risk factors, including white matter lesions and arterial stiffness [adjusted odds ratio (OR) = 4.786, 95% confidence interval (CI) = 1.710-13.39]. A multivariate analysis indicated that the albumin to globulin (A/G) ratio was the only factor that significantly lowered CD risk (OR = 0.092, 95% CI = 0.010-0.887). A/G ratio also was positively correlated with MMSE scores and negatively correlated with disruption of homeostatic factors (i.e., non-high-density lipoprotein, hemoglobin A1c, and high-sensitive C-reactive protein). Conclusions: The current study results suggest that the A/G ratio is related to cognitive decline and may reflect homeostatic alterations.
MeSH term(s)	Aged ; Aging/psychology ; C-Reactive Protein/metabolism ; Case-Control Studies ; Cognitive Dysfunction/blood ; Female ; Globulins/metabolism ; Homeostasis ; Humans ; Male ; Middle Aged ; Neuropsychological Tests ; Risk Factors ; Serum Albumin/metabolism
Chemical Substances	Globulins ; Serum Albumin ; C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2016-12-08
Publishing country	England
Document type	Journal Article
ISSN	1471-2377
ISSN (online)	1471-2377
DOI	10.1186/s12883-016-0776-z
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Article ; Online: Involvement of activated prorenin in the pathogenesis of slowly progressive nephropathy in the non-clipped kidney of two kidney, one-clip hypertension.

Ryuzaki, Masaki / Ichihara, Atsuhiro / Ohshima, Yoichi / Sakoda, Mariyo / Kurauchi-Mito, Asako / Narita, Tatsuya / Kinouchi, Kenichiro / Murohashi-Bokuda, Kanako / Nishiyama, Akira / Itoh, Hiroshi

Hypertension research : official journal of the Japanese Society of Hypertension

2011 Volume 34, Issue 3, Page(s) 301–307

Abstract: The handle region peptide (HRP), a (pro)renin receptor (P)RR blocker, did not prevent the acute nephropathy occurring 2 weeks after clipping in renovascular hypertensive rats. This study was performed to examine the effects of HRP, its scramble peptide, ... ...

Abstract	The handle region peptide (HRP), a (pro)renin receptor (P)RR blocker, did not prevent the acute nephropathy occurring 2 weeks after clipping in renovascular hypertensive rats. This study was performed to examine the effects of HRP, its scramble peptide, or a saline vehicle on slowly progressive nephropathy occurring in the kidneys of two-kidney, one-clip Goldblatt hypertensive rats. At 2 weeks after clipping, the renal morphology in the clipped and non-clipped kidneys was similar in the three groups of rats. At 12 weeks after clipping, however, the glomerulosclerosis index (GI) and the tubulointerstitial damage (TD) of the non-clipped kidneys of the HRP-treated rats were significantly lower than those of vehicle-treated rats, although the GI and the TD were similar in the rats treated with scramble peptide and vehicle. The GI and the TD of the clipped kidneys were similar in the three groups of rats at 12 weeks after clipping. In the non-clipped kidneys at 12 weeks after clipping, activated prorenin levels, angiotensin II levels and transforming growth factor (TGF)-β mRNA levels of HRP-treated rats were significantly lower than those of vehicle-treated rats, although they were similar in the non-clipped kidneys from the rats treated with scramble peptide and vehicle. In the clipped kidneys at 12 weeks after clipping, activated prorenin levels, angiotensin II levels and TGF-β mRNA levels were similar in the three groups of rats. These results suggest that the ((P)RR)-dependent activation of prorenin contributes to the pathogenesis of slowly progressive nephropathy in the intact kidney in a rat model of renovascular hypertension.
MeSH term(s)	Angiotensin II/antagonists & inhibitors ; Angiotensin II/blood ; Animals ; Disease Progression ; Hypertension, Renovascular/pathology ; Hypertension, Renovascular/physiopathology ; Kidney Diseases/drug therapy ; Kidney Diseases/pathology ; Kidney Diseases/physiopathology ; Male ; Oligopeptides/therapeutic use ; Rats ; Rats, Sprague-Dawley ; Renin/antagonists & inhibitors ; Renin/blood ; Renin/physiology ; Transforming Growth Factor beta/antagonists & inhibitors ; Transforming Growth Factor beta/blood
Chemical Substances	Oligopeptides ; Transforming Growth Factor beta ; handle-region peptide, rat ; Angiotensin II (11128-99-7) ; Renin (EC 3.4.23.15)
Language	English
Publishing date	2011-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1175297-x
ISSN	1348-4214 ; 0916-9636
ISSN (online)	1348-4214
ISSN	0916-9636
DOI	10.1038/hr.2010.230
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Zs.A 3898: Show issues

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