Mice lacking tissue plasminogen activator and urokinase plasminogen activator genes show attenuated matrix metalloproteases activity after sciatic nerve crush

Siconolfi, Lisa B.; Seeds, Nicholas W.

doi:10.1002/jnr.10786

Cited by 36 publications

(23 citation statements)

References 38 publications

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“…The substances that can activate it are numerous, for example plasmin, which plays an important role in the process of renal interstitial fibrosis [18], and it is one of the important molecules to promote pro-MMPs’ activation [19]. Another example is urokinase-type plasminogen activator (UPA), whose upregulation is associated with the development of renal interstitial fibrosis [20], and it is also known to activate the pro-MMPs [21]. …”

Section: The Regulation Of Mmp-2 and Mmp-9 Activitymentioning

confidence: 99%

MMP-2 and 9 in Chronic Kidney Disease

Cheng

Limbu

Wang

et al. 2017

IJMS

123

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Gelatinases are members of the matrix metalloproteinase (MMPs) family; they play an important role in the degradation of the extracellular matrix (ECM). This effect is also crucial in the development and progression of chronic kidney disease (CKD). Its expression, as well as its activity regulation are closely related to the cell signaling pathways, hypoxia and cell membrane structural change. Gelatinases also can affect the development and progression of CKD through the various interactions with tumor necrosis factors (TNFs), monocyte chemoattractant proteins (MCPs), growth factors (GFs), oxidative stress (OS), and so on. Currently, their non-proteolytic function is a hot topic of research, which may also be associated with the progression of CKD. Therefore, with the in-depth understanding about the function of gelatinases, we can have a more specific and accurate understanding of their role in the human body.

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Section: The Regulation Of Mmp-2 and Mmp-9 Activitymentioning

confidence: 99%

MMP-2 and 9 in Chronic Kidney Disease

Cheng

Limbu

Wang

et al. 2017

IJMS

123

View full text Add to dashboard Cite

show abstract

“…It has been reported that tPA may be an activator of MMP-9 [19]. Mice lacking tPA genes showed a attenuated MMP-9 activity after sciatic nerve crush [20]. Our study indicated that up-regulation of tPA might induce the fibrinolytic activity and the interaction of tPA and PAI regulated the fibrinolytic activity after nerve injury.…”

Section: Discussionmentioning

confidence: 66%

The Role and Mechanism of the Up-Regulation of Fibrinolytic Activity in Painful Peripheral Nerve Injury

Nie

Cai

2008

Neurochem Res

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Peripheral nerve injury is followed by Wallerians degeneration (WD) and degradation and regeneration of the extracellular matrix (ECM) are very important events in these processes. We tested fibrinolytic activities and the expression level of tPA and uPA levels in chronic constriction injury (CCI) model. The presented data demonstrates that in the injury nerve of CCI model, the fibrinolytic activities is upregulated and main caused by the upregulation of tPA expression. We also find that the activities of tPA and MMP-9 are co-upregulated post-CCI, both at CCI site and proximal site. These results indicate that tPA activity may regulate the MMP-9 activity in injury nerve post-CCI.

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“…Activation of MMP2 and MMP9 is partially dependent on the presence of tissue PA (tPA) and/or urokinase PA (UPA) systems (Siconolfi and Seeds 2003) and the deletion of tPA and/or UPA interferes with functional recovery after peripheral nerve injury (Siconolfi and Seeds 2001). As with chondroitinase (Graham et al 2007;Hattori et al 2008;Udina et al 2010), the administration of exogenous MMP2 has been shown to degrade chondroitin sulphate proteoglycans and to improve recovery and anatomical reinnervation following nerve transection; furthermore, in the presence of saturating concentrations of MMP2, the co-administration of chondrotinase ABC does not produce any additional improvement, suggesting that both enzymes attack the same target (Zuo et al 1998a(Zuo et al , 1998b.…”

Section: Adhesion Moleculesmentioning

confidence: 99%

Downstream effector molecules in successful peripheral nerve regeneration

Patodia

Raivich

2012

Cell Tissue Res

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The robust axon regeneration that occurs following peripheral nerve injury is driven by transcriptional activation of the regeneration program and by the expression of a wide range of downstream effector molecules from neuropeptides and neurotrophic factors to adhesion molecules and cytoskeletal adaptor proteins. These regeneration-associated effector molecules regulate the actin-tubulin machinery of growth-cones, integrate intracellular signalling and stimulatory and inhibitory signals from the local environment and translate them into axon elongation. In addition to the neuronally derived molecules, an important transcriptional component is found in locally activated Schwann cells and macrophages, which release a number of cytokines, growth factors and neurotrophins that support neuronal survival and axonal regeneration and that might provide directional guidance cues towards appropriate peripheral targets. This review aims to provide a comprehensive up-to-date account of the transcriptional regulation and functional role of these effector molecules and of the information that they can give us with regard to the organisation of the regeneration program.

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Mice lacking tissue plasminogen activator and urokinase plasminogen activator genes show attenuated matrix metalloproteases activity after sciatic nerve crush

Cited by 36 publications

References 38 publications

MMP-2 and 9 in Chronic Kidney Disease

MMP-2 and 9 in Chronic Kidney Disease

The Role and Mechanism of the Up-Regulation of Fibrinolytic Activity in Painful Peripheral Nerve Injury

Downstream effector molecules in successful peripheral nerve regeneration

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