Prostaglandins increase proMMP-1 and proMMP-3 secretion by human ciliary smooth muscle cells

Lindsey, James D.; Kashiwagi, Kenji; Boyle, David; Kashiwagi, Fumiko; Firestein, Gary S.; Weinreb, Robert N.

doi:10.3109/02713689609017628

Cited by 146 publications

(77 citation statements)

References 31 publications

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“…Their earlier work had shown that following treatment of human ciliary muscle cells in culture with PGF 2α , collagens type I and III were reduced while matrix metalloproteinases 1, 2, 3 and 9 were increased (Lindsey et al, 1996;Lindsey et al, 1997). In vivo, following topical treatment of monkey eyes for 5 days with PGF 2α , collagen types I, III, and IV immunoreactivity in the ciliary muscle and adjacent sclera was reduced (Sagara et al, 1999) while matrix metalloproteinases 1, 2, and 3 were increased (Table 1) (Gaton et al, 2001;Weinreb et al, 2002).…”

Section: Prostaglandins and Enhancement Of Uveoscleral Outflowmentioning

confidence: 99%

Enhancing trabecular outflow by disrupting the actin cytoskeleton, increasing uveoscleral outflow with prostaglandins, and understanding the pathophysiology of presbyopia

Kaufman

2008

Experimental Eye Research

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Several major areas of work by the author and his international collaborators are reviewed. 1) The ciliary muscle in the nonhuman primate eye was disinserted at the scleral spur. Pilocarpine was then ineffective in increasing outflow facility, indicating that ciliary muscle contraction mediated the IOPlowering effect of muscarinic cholinergics. 2) Compounds such as cytochalasins, H-7 and latrunculin A/B, which alter the actin cytoskeleton, cellular contractility and cellular adhesions in cultured trabecular meshwork cells, relaxed trabecular pathway cells and consequently the meshwork itself so as to decrease IOP and enhance trabecular outflow facility in nonhuman primates. Gene transfer approaches utilizing C3 and caldesmon over-expression by viral vectors to target specific steps in the cellular contractility/cytoskeleton/cell adhesion cascades characteristically altered trabecular meshwork cell morphology and increased outflow facility in organ-cultured anterior segments. 3) Prostaglandin F 2α analogues enhanced matrix metalloproteinase production by ciliary muscle cells and scleral fibroblasts, leading to remodeling of the extracellular matrix of the ciliary muscle and sclera and consequently to increased uveoslceral outflow and decreased IOP in primates. 4) The rhesus monkey was an excellent model for human presbyopia, losing the accommodative response to cholinergic stimulation in the same timeframe relative to lifespan. No changes were found in ciliary muscle enzymes involved in acetylcholine biosynthesis or degradation or in muscarinic receptor numbers or affinity. Contractility of isolated ciliary muscle did not diminish with age, but posterior ciliary muscle attachments stiffened, suggesting a possible role in restricting muscle and consequently lens movement during accommodation. A model to reproducibly stimulate accommodation through central stimulation of the Edinger-Westphal nucleus was developed. Goniovideography and ultrasound biomicroscopic techniques allowed real-time recording and analysis of the accommodation-relevant structures. Surgical ablation of the intraocular structures involved in the accommodation response has led to further understanding of their roles and changes with age related to presbyopia. 5) Global collaborations such as those involved in these studies will be essential in the future, as science becomes "bigger".Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The story I will tell is embodied in the title. It is about recognizing questions, asking how and why things happen, recognizing signs along the way, and about focus yet w...

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Section: Prostaglandins and Enhancement Of Uveoscleral Outflowmentioning

confidence: 99%

Enhancing trabecular outflow by disrupting the actin cytoskeleton, increasing uveoscleral outflow with prostaglandins, and understanding the pathophysiology of presbyopia

Kaufman

2008

Experimental Eye Research

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“…PGE is involved in stimulating MMP production (Lindsey et al, 1996;Zeng et al, 1996;Shankavaram et al, 1997), stimulation of IL-8 and IL-10 production (Strassmann et al, 1994;Agro et al, 1996;Denison et al, 1999), antibody class switching in B cells (Phipps et al, 1991;Roper et al, 1990) and inhibition of IL-12 synthesis from activated monocytes (Kraan et al, 1995). All of these properties of PGE are consistent with the damping of any Th-1 (cellmediated) response within decidua, where a major source of PGE would be the trophoblast (Kelly et al, 1995).…”

Section: Prostaglandinsmentioning

confidence: 99%

Cytokine control in human endometrium

Kelly

King²,

Critchley³

2001

Reproduction

209

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Critical reproductive events in endometrium such as menstruation and implantation have an inflammatory character (Finn, 1986). Menstruation and implantation involve both prostaglandins and cytokines and are accompanied by the ingress of leucocytes into the endometrium. Moreover, oedema is characteristic of endometrium both premenstrually and at the time of implantation. Endometrial physiology relating to these events is still poorly understood and this ignorance hinders better medical approaches to major pathologies of menstruation, such as menorrhagia and dysmenorrhoea, and failure of implantation.One of the most revealing studies on the mechanism of menstruation was published 60 years ago by Markee (1940) who transplanted endometrium to the anterior chamber of the monkey eye, where events surrounding menstruation could be observed microscopically. The early events of menstruation involve vasoconstriction of the spiral blood vessels followed by a relaxation of the arterioles and reperfusion of the tissue. Prolonged periods of vasoconstriction that would have induced hypoxia and the inevitable reperfusion injury were also observed. Such periods of vasoconstriction have not been confirmed in women in studies with techniques such as Doppler flow (Gannon et al., 1997) and xenon clearance (Fraser et al., 1987), but such techniques are unlikely to detect highly localized changes. Hypoxia would certainly be a sufficient cause of cytokine release since hypoxia affects the NFκB pathway (Royds et al., 1998) and many genes have hypoxic response elements. Re-exposure to oxygen is likely to be accompanied by an upregulation of cytokine (Karakurum et al., 1994) matrix metalloproteinase (MMP) (Fujimura et al., 1999; Heo et al., 1999) vascular endothelial growth factor (VEGF) (Goldberg and Schneider, 1994;Sharkey et al., 2000) and prostaglandin (Kishimoto et al., 1997) production. However, the events preceding vasoconstriction are less clear. The early events in menstruation are initiated by the withdrawal of the circulating progesterone as a result of the demise of the corpus luteum and are likely to involve cells close to the spiral arterioles where the constriction Cytokines within endometrium participate in both menstruation and implantation but also contribute to the defence mechanisms of the mucosal epithelium. Endometrium is under the control of steroid hormones, particularly progesterone and, thus, control of cytokines by this steroid is important. Although appreciable numbers of progesterone receptors are not found in endometrial leucocytes, progesterone can modulate cytokines by acting on uterine cells expressing the receptor. The NFκB pathway is important in the control of cytokine synthesis and can modulate production of chemokines, matrix metalloproteinases and the inducible prostaglandin synthesis enzyme COX-2. NFκB activity can be inhibited by progesterone by either stimulating synthesis of IκB, the molecule that restrains NFκB in the cytosol, or after binding to the nuclear receptor, competing with NFκB for ...

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“…9,11 In addition, a reduction in collagen types I, III, and IV in PGF 2␣ -treated human ciliary muscle cultures have been reported. 14 Further, a reduction in these collagens was observed in the ciliary muscle of inflamed monkey eyes previously treated with PGF 2␣ -IE, in which uveoscleral outflow was also increased.…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10][11][12][13][14][15] Although studies have shown that MMPs can alter conventional outflow facility in human and animal perfused eyes, 16,17 direct evidence that MMPs participate in the FPagonist-induced modulation of IOP remains to be determined.…”

mentioning

confidence: 99%

Latanoprost-Induced Changes in Rat Intraocular Pressure: Direct or Indirect?

Husain

Yates

Crosson

2008

Journal of Ocular Pharmacology and Therapeutics

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Introduction: The topical application of prostaglandin F 2␣ (FP)-receptor agonists has been shown to significantly lower intraocular pressure (IOP) in humans and is now considered the first-line treatment for ocular hypertension. Despite the prominent role FP-receptor agonists play in the treatment of glaucoma, our understanding of how these agents lower IOP remains incomplete. The present study was designed to evaluate the role of matrix metalloproteinase (MMP) activation and the cytokine, tumor necrosis factor alpha (TNF-␣), in latanoprost-induced changes in IOP. Methods: Changes in IOP following an acute topical administration of latanoprost (60 ng) in normotensive Brown Norway rats were evaluated by means of a commercially available rebound tonometer. To examine the role of MMPs and TNF-␣ in this response, the rats were pretreated with a broad-spectrum MMP inhibitor, GM-6001 (100 g), or the TNF-␣ inhibitor, thalidomide (25 g). Results: The topical administration of latanoprost (60 ng) alone produced a biphasic change in ipsilateral IOP: an initial hypertension (4.21 Ϯ 0.52), followed by a prolonged hypotension (Ϫ4.79 Ϯ 0.65). In rats, pretreatment with GM-6001 blocked the latanoprost-induced reduction in IOP but did not prevent the initial rise in IOP. Pretreatment with thalidomide also blocked the ocular hypotension induced by latanoprost; however, thalidomide pretreatment enhanced the duration of the initial hypertension. Conclusions: These results provide evidence that the secretion and activation of MMPs and the release of TNF-␣ play a central role in the ocular hypotension induced by FP-agonists. The administration of FP-agonists appears to lower IOP directly by inducing the activation of MMPs within the ciliary body, leading to improved uveoscleral outflow and indirectly through the release of TNF-␣ within the ciliary body. Secreted TNF-␣ may then activate TNF-receptors in the uvea and trabecular meshwork, increasing both uveoscleral and conventional outflow.

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Prostaglandins increase proMMP-1 and proMMP-3 secretion by human ciliary smooth muscle cells

Abstract: These results suggest that induction of MMPs in situ following topical PG treatment may degrade ciliary muscle extracellular matrix and possibly contribute to increased uveoscleral outflow, as well.

Cited by 146 publications

References 31 publications

Enhancing trabecular outflow by disrupting the actin cytoskeleton, increasing uveoscleral outflow with prostaglandins, and understanding the pathophysiology of presbyopia

Enhancing trabecular outflow by disrupting the actin cytoskeleton, increasing uveoscleral outflow with prostaglandins, and understanding the pathophysiology of presbyopia

Cytokine control in human endometrium

Latanoprost-Induced Changes in Rat Intraocular Pressure: Direct or Indirect?

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