Cystic vestibular schwannomas: a possible role of matrix metalloproteinase–2 in cyst development and unfavorable surgical outcome

2007 ◽  
Vol 106 (5) ◽  
pp. 866-871 ◽  
Author(s):  
Kyung-Sub Moon ◽  
Shin Jung ◽  
Seung-Kwon Seo ◽  
Tae-Young Jung ◽  
In-Young Kim ◽  
...  

Object The authors evaluated the clinical manifestations and surgical results in patients with cystic vestibular schwannoma (VS), and investigated the matrix metalloproteinase (MMP) expression of the cyst fluid and wall in an attempt to elucidate the pathogenesis and characteristics of this disease. Methods The clinical and neuroimaging features, perioperative findings, and surgical outcomes in 24 cases of cystic VS and 82 cases of solid VS, all of which were treated using the suboccipital approach, were retrospectively compared. To evaluate the role of MMP in cystic VS, gelatin zymography and immunohistochemical studies of the cyst fluid, wall, and solid portion were performed in nine cases of this disease. The mean duration of symptoms was shorter (14.0 months compared with 26.1 months; p = 0.04) and the mean size of the tumor was larger (43.8 mm compared with 34.2 mm; p = 0.048) in the cystic than the solid VS group. Although gross-total resection was easier to accomplish in this group (100% compared with 84.1%), adhesion to the facial nerve was more frequent (62.5% compared with 48.8%; p = 0.042). On gelatin zymography studies, MMP-2 expression was ubiquitously observed in all cyst fluids. Immunohistochemical analysis of the cyst wall showed that MMP-2 was apparently localized to the tumor cells on the luminal inner surface, adjacent to the cyst cavity. Conclusions Resection of cystic VS is complicated by severe adhesion of the tumor capsule to the facial nerve and the large size of the lesion. The authors believe that MMP-2 may be involved in the pathogenesis of cyst formation or in its enlargement and may aggravate adhesion to the facial nerve, either by promoting the enlargement of the tumor or engendering the degradation of the tumor–nerve barrier proteolytically.

2021 ◽  
Vol 41 ◽  
pp. 100959
Author(s):  
Long-Jie Yan ◽  
Le-Chang Sun ◽  
Kai-Yuan Cao ◽  
Yu-Lei Chen ◽  
Ling-Jing Zhang ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-3 ◽  
Author(s):  
Talvensaari-Mattila Anne ◽  
Turpeenniemi-Hujanen Taina

Background. The role of matrix metalloproteinase-2 and -9 (MMP-2, MMP-9) in matrix degradation and metastasis has been described in various tumors. Their action is inhibited by their natural tissue inhibitor molecules TIMP-1 and -2.Methods. The study population consisted of 12 squamous cervical carcinoma patients and 27 healthy volunteer control patients. MMP-9, MMP-2-TIMP-2 complex, TIMP-1, and TIMP-2 were analyzed from serum samples using enzyme-linked immunoassay (ELISA).Results. The mean levels of serum TIMP-2 and of MMP-2-TIMP-2 complex were higher in healthy controls compared to patients with a malignant tumor. Serum TIMP-2 values decreased significantly from healthy controls (median 323 g/l, range 305–342 g/l) to malignant (median 136 g/l, range 120–151 g/l) squamous cervical carcinoma patients . Also, serum proMMP2-TIMP2 complex values decreased from control patients to squamous cervical carcinoma patients .Conclusion. This paper shows that the levels of circulating TIMP-2 and that of MMP-2-TIMP-2 complex are lower in squamous cervical carcinoma patients than in healthy women.


2019 ◽  
Vol 316 (1) ◽  
pp. C92-C103 ◽  
Author(s):  
Hojin Kang ◽  
Zhigang Hong ◽  
Ming Zhong ◽  
Jennifer Klomp ◽  
Kayla J. Bayless ◽  
...  

Angiogenesis is initiated in response to a variety of external cues, including mechanical and biochemical stimuli; however, the underlying signaling mechanisms remain unclear. Here, we investigated the proangiogenic role of the endothelial mechanosensor Piezo1. Genetic deletion and pharmacological inhibition of Piezo1 reduced endothelial sprouting and lumen formation induced by wall shear stress and proangiogenic mediator sphingosine 1-phosphate, whereas Piezo1 activation by selective Piezo1 activator Yoda1 enhanced sprouting angiogenesis. Similarly to wall shear stress, sphingosine 1-phosphate functioned by activating the Ca2+ gating function of Piezo1, which in turn signaled the activation of the matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase during sprouting angiogenesis. Studies in mice in which Piezo1 was conditionally deleted in endothelial cells demonstrated the requisite role of sphingosine 1-phosphate-dependent activation of Piezo1 in mediating angiogenesis in vivo. These results taken together suggest that both mechanical and biochemical stimuli trigger Piezo1-mediated Ca2+ influx and thereby activate matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase and synergistically facilitate sprouting angiogenesis.


2018 ◽  
Vol 9 ◽  
Author(s):  
Yu Kuwabara ◽  
Tetsu Kobayashi ◽  
Corina N. D'Alessandro-Gabazza ◽  
Masaaki Toda ◽  
Taro Yasuma ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Binbin Zheng ◽  
Hongbo Yang ◽  
Jianan Zhang ◽  
Xueli Wang ◽  
Hao Sun ◽  
...  

Acute lung injury (ALI) is one of the fatal symptoms of sepsis. However, there were no effective clinical treatments. TF accumulation-induced fibrin deposit formations and coagulation abnormalities in pulmonary vessels contribute to the lethality of ALI. Suppressor of cytokine signaling 3 (SOCS3) acts as an endogenous negative regulator of the TLR4/TF pathway. We hypothesized that inducing SOCS3 expression using lidocaine to suppress the TLR4/TF pathway may alleviate ALI. Hematoxylin and eosin (H&E), B-mode ultrasound, and flow cytometry were used to measure the pathological damage of mice. Gelatin zymography was used to measure matrix metalloproteinase-2/9 (MMP-2/9) activities. Western blot was used to assay the expression of protein levels. Here, we show that lidocaine could increase the survival rate of ALI mice and ameliorate the lung injury of ALI mice including reducing the edema, neutrophil infiltration, and pulmonary thrombosis formation and increasing blood flow velocity. Moreover, in vitro and in vivo, lidocaine could increase the expression of p-AMPK and SOCS3 and subsequently decrease the expression of p-ASK1, p-p38, TF, and the activity of MMP-2/9. Taken together, our study demonstrated that lidocaine could inhibit the TLR4/ASK1/TF pathway to alleviate ALI via activating AMPK-SOCS3 axis.


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