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Articles by K Miyata
Total Records ( 2 ) for K Miyata
  N Honda , T Miyai , R Nejima , K Miyata , T Mimura , T Usui , M Aihara , M Araie and S. Amano
 

Objective  To investigate the effect of topical latanoprost on the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinase 1 (TIMP-1) on the ocular surface.

Methods  Tears were collected from 39 patients with glaucoma who used latanoprost, 0.005%, eyedrops (Xalatan) and 28 healthy volunteers. The MMP-9 concentration was measured. Conjunctival epithelial cells were collected from 10 eyes of 10 patients before and 1 to 3 months after starting to take topical latanoprost, 0.005%, and MMP-1, MMP-9, and TIMP-1 messenger RNA (mRNA) expression was analyzed. Both eyes of 48 mice were treated once a day with latanoprost, 0.005%, timolol gel, 0.5%, eyedrops, vehicle of Xalatan, or phosphate-buffered saline, and MMP-9 and TIMP-1 mRNA expression was analyzed.

Results  The median MMP-9 concentration in latanoprost-treated cases was 91.2 ng/mL (in controls, 19.7 ng/mL; P < .001). In latanoprost-treated cases, the relative ratio of MMP-9 to glyceraldehyde 3-phosphate dehydrogenase mRNA was significantly increased from 6.42 to 21.3 (P = .04, paired t test) and the relative amount of TIMP-1 was significantly decreased from 154 to 105 (P = .009). The relative amount of MMP-1 to GAPDH mRNA before and after latanoprost use was not significantly different (P = .16). In mice, MMP-9 expression was increased and TIMP-1 expression was decreased on the ocular surface at 8 weeks after latanoprost use.

Conclusion  The topical use of latanoprost increases MMP-1 and MMP-9 and decreases TIMP-1 on the ocular surface.

Clinical Relevance  The use of topical latanoprost might not be recommended in patients with keratoconus or after laser-assisted in situ keratomileusis.

  R Satou , K Miyata , A Katsurada , L. G Navar and H. Kobori
 

Angiotensinogen (AGT) expression in renal proximal tubular cells (RPTCs) and intrarenal tumor necrosis factor- (TNF-) levels are increased in hypertension and renal diseases However, the contribution of TNF- to AGT expression in RPTCs has not been established. Therefore, the objective of the present study was to determine influence of TNF- on AGT expression in RPTCs. Human kidney-2 (HK-2) cells, immortalized human RPTCs, were treated with several concentrations of TNF- up to 24 h. AGT mRNA and protein expression were evaluated by RT-PCR and ELISA, respectively. Activation of nuclear factor-B (NF-B) by TNF- was evaluated by Western blot analysis, immunocytochemistry, and electrophoretic mobility shift assay (EMSA). TNF- suppressed AGT mRNA expression in a dose- and time-dependent manner. Maximum AGT mRNA reduction was caused by 40 ng/ml of TNF- (0.52 ± 0.09, ratio to control, at 24 h) and at 24 h (0.66 ± 0.05, ratio to control, by 10 ng/ml TNF-). TNF- reduced AGT protein accumulation in the medium between 8 and 24 h (0.62 ± 0.13 by 40 ng/ml TNF-, ratio to control). TNF- activated and induced translocalization of p50 and p65, which are NF-B subunits. Elevated formation of p50/p65 and p50/p50 dimers by TNF- were observed by EMSA and supershift assay. Gene silencing of p50, but not p65, attenuated the effect of TNF- on reduction of AGT expression in RPTCs. These results indicate that TNF- suppresses AGT expression through p50/p50 homodimer formation in human RPTCs, suggesting a possible counteracting mechanism that limits excessive intrarenal AGT production.

 
 
 
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