Decrease of MMP-9 Activity Improves Soleus Muscle Regeneration

Zimowska, Małgorzata; Olszyński, Krzysztof H.; Swierczynska, Marta M.; Stremińska, Władysława; Ciemerych, Maria A.

doi:10.1089/ten.tea.2011.0459

Cited by 36 publications

(44 citation statements)

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“…MMP antibodies and inhibitors can also be used to elucidate the exact roles that they play in bladder regeneration. 38,43 In the present study, we found the difference of smooth muscle regeneration and vascularization between the marginal and central zones of tissue-engineered neobladder. Furthermore, smooth muscle regeneration and vascularization of tissue-engineered neobladder were still insufficient to obtain the recovery of contractive function of bladder tissues and maintain bladder function compared with native bladder.…”

Section: Discussionsupporting

confidence: 59%

“…[36][37][38] It is reported that MMPs play a critical role on the regeneration of skeletal muscle, liver, cartilage, bone, and angiogenesis when the tissue-engineering approaches are utilized for tissue repair. 36,37,[39][40][41][42][43][44] In addition, some studies indicated that both smooth muscle cells and urothelial cells could secret MMP-2 and MMP-9 in vitro. 45,46 In the present study, the native bladder tissues around the reconstruction area were retrieved to evaluate the MMPs.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Coadministration of Platelet-Derived Growth Factor-BB and Vascular Endothelial Growth Factor with Bladder Acellular Matrix Enhances Smooth Muscle Regeneration and Vascularization for Bladder Augmentation in a Rabbit Model

Zhou

Yang²,

Sun³

et al. 2013

Tissue Engineering Part A

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Coadministration of Platelet-Derived Growth Factor-BB and Vascular Endothelial Growth Factor with Bladder Acellular Matrix Enhances Smooth Muscle Regeneration and Vascularization for Bladder Augmentation in a Rabbit Model

Zhou

Yang²,

Sun³

et al. 2013

Tissue Engineering Part A

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“…It has recently been demonstrated that Doxy can be beneficial for mdx mice mainly by reducing MMP-9 and TNF- α expression [15]. It was also demonstrated that Doxy or anti-MMP-9 antibody improves soleus muscle regeneration and ameliorate development of excessive fibrosis [16]. In addition, recent work showed that Doxy treatment can regulate both local and systemic inflammation, suggesting its importance in inflammatory myopathies [17, 18].…”

Section: Introductionmentioning

confidence: 99%

Doxycycline Inhibits IL-17-Stimulated MMP-9 Expression by Downregulating ERK1/2 Activation: Implications in Myogenic Differentiation

Obradović

Krstić

Кукољ

et al. 2016

Mediators of Inflammation

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Interleukin 17 (IL-17) is a cytokine with pleiotropic effects associated with several inflammatory diseases. Although elevated levels of IL-17 have been described in inflammatory myopathies, its role in muscle remodeling and regeneration is still unknown. Excessive extracellular matrix degradation in skeletal muscle is an important pathological consequence of many diseases involving muscle wasting. In this study, the role of IL-17 on the expression of matrix metalloproteinase- (MMP-) 9 in myoblast cells was investigated. The expression of MMP-9 after IL-17 treatment was analyzed in mouse myoblasts C2C12 cell line. The increase in MMP-9 production by IL-17 was concomitant with its capacity to inhibit myogenic differentiation of C2C12 cells. Doxycycline (Doxy) treatment protected the myogenic capacity of myoblasts from IL-17 inhibition and, moreover, increased myotubes hypertrophy. Doxy blocked the capacity of IL-17 to stimulate MMP-9 production by regulating IL-17-induced ERK1/2 MAPK activation. Our results imply that MMP-9 mediates IL-17's capacity to inhibit myoblast differentiation during inflammatory diseases and indicate that Doxy can modulate myoblast response to inflammatory induction by IL-17.

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“…11,12 While our findings indicate that doxy inhibits injury associated MMP-8 activity, other proteases, such as MMP-9 or MMP-13 may also be modulated by doxy treatment. 24,30 The effects of doxy on other Type I collagenases (MMP-1 or MMP-13) or other proteases were not explored. It is also unknown if doxy modulates activity of endogenous TIMPs, known to be regulated in tendon injury.…”

mentioning

confidence: 99%

Enhancement of Achilles tendon repair mediated by matrix metalloproteinase inhibition via systemic administration of doxycycline

Kessler

Barr

Greenwald

et al. 2013

Journal Orthopaedic Research

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Collagenases or matrix metalloproteinases (MMPs) have been shown to play an important role in the matrix degradation cascade associated with Achilles tendon rupture and disease. The goal of this study was to examine the effects of daily administration of doxycycline (Doxy) through oral gavage on MMP activity and on the repair quality of Achilles tendons in vivo. Our findings indicate that Achilles tendon transection resulted in increasing MMP-8 activity from 2 to 6 weeks post-injury, with peak increases in activity occurring at 4 weeks post-injury. Doxy adiministration at clinically relevant serum concentrations was found to significantly inhibit MMP activity after continuous treatment for 4 weeks, but not for continuous administration for shorter durations (96 h or 2 weeks). Extended doxy administration was also associated with improved collagen fibril organization, and enhanced biomechanical properties (stiffness, ultimate tensile strength, maximum load to failure, and elastic toughness). Our findings indicate that a temporal delay exists between Achilles tendon transection and associated increases in MMP-8 activity in situ. Our findings suggest that inhibition of MMP-8 at its peak activity levels ameliorates fibrosis development and improves biomechanical properties of the Achilles tendon. Keywords: achilles tendon; matrix metalloproteinase; doxycycline; tendon rupture and repair Achilles tendon tears are devastating injuries, and have unpredictable outcomes with respect to return to function.1,2 Collagenases or matrix metalloproteinases (MMPs) have been shown to play an important role in the enzymatic matrix degradation cascade associated with tendon injury and disease.3-6 Tendon degeneration is an active, cell-mediated process that may result from a failure to regulate specific MMP activities in response to repeated injury or mechanical strain. After tendon rupture, increased activity of MMPs and increased matrix turnover have been associated with further deterioration in the quality of the collagen network.7-13 Downregulation of tissue inhibitors of MMPs (TIMPS) is also associated with disregulation of the ratio of MMP to TIMP activity, and has been implicated in the pathogenesis of tendinopathy. [8][9][10][11][12][13][14][15][16] Tenocyte production of MMP-1 and -3 underscores the potential for non-lymphocyte mediated cytokine production of proteases inducing local matrix changes. 17 Tetracyclines, through a mechanism independent of their antibiotic effects, have been shown to substantially inhibit the action of MMPs, such as collagenase.18-21 Specifically, doxycycline (doxy) is considered to be the most potent tetracycline MMP inhibitor, whose activity is mediated both by direct and indirect mechanisms of action, and has been applied therapeutically in a variety of clinical applications.18-21 The use of doxy in tendon repair had been previously explored in vivo, though contradictory findings regarding its efficacy have been reported. [22][23][24] Consequently, MMP inhibitors and their activity ...

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Decrease of MMP-9 Activity Improves Soleus Muscle Regeneration

Cited by 36 publications

References 44 publications

Coadministration of Platelet-Derived Growth Factor-BB and Vascular Endothelial Growth Factor with Bladder Acellular Matrix Enhances Smooth Muscle Regeneration and Vascularization for Bladder Augmentation in a Rabbit Model

Coadministration of Platelet-Derived Growth Factor-BB and Vascular Endothelial Growth Factor with Bladder Acellular Matrix Enhances Smooth Muscle Regeneration and Vascularization for Bladder Augmentation in a Rabbit Model

Doxycycline Inhibits IL-17-Stimulated MMP-9 Expression by Downregulating ERK1/2 Activation: Implications in Myogenic Differentiation

Enhancement of Achilles tendon repair mediated by matrix metalloproteinase inhibition via systemic administration of doxycycline

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