| Regulation of Matrix Metalloproteinase 2 Expression by an Adenosine A1 Agonist in Trabecular Meshwork Cells. |
|
Min Ju Baek, Keun Hae Kim, Jae Woo Kim |
|
Department of Ophthalmology, Daegu Catholic University School of Medicine, Daegu, Korea. jwkim@cu.ac.kr |
| 섬유주세포에서 아데노신 A1 길항제에 의한 기질단백분해효소 2의 발현 조절 |
|
백민주⋅김근해⋅김재우 |
|
대구가톨릭대학교 의과대학 안과학교실 |
Correspondence:
Jae Woo Kim,
Email: jwkim@cu.ac.kr
|
|
Received: 30 November 2017 • Revised: 12 December 2017 • Accepted: 28 September 2018 |
| Abstract |
PURPOSE
We investigated the extent of adenosine A1 agonist-induced expression and regulation of matrix metalloproteinase 2 (MMP-2) synthesis in human trabecular meshwork cells (HTMC). METHODS: Primary HTMC cultures were exposed to 0.1 or 1.0 µM N6-cyclohexyladenosine (CHA) for 2 h in the presence or absence of an inhibitor thereof, 8-cyclopentyl-1,3-dimethylxanthine (CPT). The expression level of mRNA encoding MMP-2 was assessed via reverse transcription-polymerase chain reaction, and the levels of tissue inhibitor of metalloproteinase 2 (TIMP2) and membrane-type-1 MMP (MT1-MMP) measured by Western blotting. The permeability of the HTMC monolayer was assessed with the aid of carboxyfluorescein. RESULTS: CHA at 1.0 µM increased the permeability of the HTMC monolayer (p = 0.003) and CHA at both 0.1 and 1.0 µM significantly increased MMP-2 mRNA expression, which was inhibited by co-exposure to CPT (all p < 0.05). CHA increased MMP-2 activity, decreased that of TIMP2, and increased that of MT1-MMP (all p < 0.05). CONCLUSIONS: CHA increased the permeability of the HTMC monolayer and increased MMP-2 activity, decreased TIMP2 activity, and increased MT1-MMP activity. Thus, regulation of TIMP2 and MT1-MMP expression may be involved in the adenosine A1 agonist-induced increase in MMP-2 activity. |
| Key Words:
Adenosine A1 agonist;Matrix metalloproteinase 2;Permeability;Trabecular meshwork |
|
PDF Links
Full text via DOI
Download Citation
