Rho Kinase Type 1 (ROCK1) Promotes Lipopolysaccharide-induced Inflammation in Corneal Epithelial Cells by Activating Toll-Like Receptor 4 (TLR4)-Mediated Signaling

Gong, Jianying; Guan, Lan; Tian, Peng; Li, Chao; Zhang, Yi

doi:10.12659/msm.907277

Cited by 17 publications

(12 citation statements)

References 24 publications

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“…Previous studies suggested that nuclear factor-κB (NF-κB) signaling is an important pathway for the development of gastric cancer and ROCK1 is a key mediator of this spathway. [29][30][31][32] Hence, we hypothesized that NF-κB signaling might be involved in the regulatory mechanism addressed by circNRIP1/miR-182/ROCK1 axis in gastric cancer, which is needed to be explored in the future.…”

Section: Discussionmentioning

confidence: 99%

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

Liang

2020

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Aim: Circular RNAs (circRNAs) play important roles in the progression of human cancers. circRNA nuclear receptor interacting protein 1 (circNRIP1) has been reported to play as an oncogene in gastric cancer. However, the mechanism underlying circNRIP1 in gastric cancer progression is far from understood. Patients and Methods: Forty-five gastric cancer patients were recruited and overall survival of patients was analyzed. Gastric cancer cell lines MGC-803 and AGS cells were cultured for study in vitro. The expression levels of circNRIP1, microRNA (miR)-182 and rho-associated protein kinase 1 (ROCK1) were detected by quantitative real-time polymerase chain reaction or Western blot. Cell migration, invasion, cell cycle distribution and apoptosis were determined by transwell, flow cytometry and Western blot assays, respectively. The target association between miR-182 and circNRIP1 or ROCK1 was assessed by luciferase reporter assay and RNA immunoprecipitation. Results: circNRIP1 expression was enhanced in gastric cancer tissues and cells and high expression of circNRIP1 indicated poor survival of patients. Knockdown of circNRIP1 suppressed cell migration and invasion, arrested cell cycle at G0-G1 phase and promoted apoptosis in gastric cancer cells. miR-182 was a target of circNRIP1 and its deficiency reversed the effect of circNRIP1 silence on cell migration, invasion, cell cycle distribution and apoptosis in gastric cancer cells. Moreover, ROCK1 was validated as a target of miR-182 and competitively regulated by circNRIP1. Conclusion: Silence of circNRIP1 inhibited progression of gastric cancer by increasing miR-182 and decreasing ROCK1, providing a novel target for the treatment of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

Liang

2020

OTT

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“…11,48,49 Past studies have reported a correlation between TNF-α and ROCK; TNF-α induced activated Rho, whereas ROCK promoted translocation of NF-κB to the nucleus to accelerate the production of TNF-α. 50,51 Based on these results, we speculated that higher expression of TNF-α induced CMV-infected hCECs and active RhoA, resulting in translocation of NF-κB to the nucleus to induce apoptosis. Also, NF-κB translocation to the nucleus may accelerate the production of TNF-α to maintain RhoA in an activated state.…”

Section: Discussionmentioning

confidence: 96%

“…In corneal endothelial cells, it has been reported that overexpression of ROCK1 may trigger lipopolysaccharide-induced production of TNF-α and its downstream apoptosis, which could be attenuated with ROCK inhibitors. 51 Yang et al 50 reported a preservative effect of ROCK inhibitors on the apoptosis of microvascular endothelial cells via inhibition of the nuclear translocation of NF-κB and consequent suppression of the generation of TNF-α. We therefore hypothesize that ROCK inhibitors may modulate the CMV-infection-induced generation of TNF-α.…”

Section: Discussionmentioning

confidence: 99%

Effects of ROCK Inhibitors on Apoptosis of Corneal Endothelial Cells in CMV-Positive Posner–Schlossman Syndrome Patients

Igarashi

Honjo

Kaburaki

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. To examine the role of aqueous tumor necrosis factor α (TNF-α)-RhoA-Rho kinase (ROCK) signaling in cytomegalovirus (CMV)-induced apoptosis and the barrier function of cultured human corneal endothelial cells (hCECs) in CMV-positive Posner-Schlossman syndrome (CMV+/PSS) patients. METHODS. Aqueous levels of TNF-α, IL-8, IL-10, and several other cytokines in 19 CMV+/PSS patients and 20 healthy control subjects were quantitated using a multiplex assay. The expression of active RhoA in hCECs post-CMV infection was determined using western blotting (WB). The expression levels of TNF-α and nuclear factor kappa B (NF-κB) in CMV-infected hCECs were examined by immunocytochemistry (ICC) and WB with and without ROCK inhibitors. The apoptotic rate and barrier integrity in CMV-infected hCECs were also examined. RESULTS. The expression levels of TNF-α, monocyte chemoattractant protein-1 (MCP-1), IL-8, and IL-10 were upregulated in the aqueous humor of CMV+/PSS patients, and among these upregulated cytokines aqueous TNF-α was negatively correlated with the number of corneal endothelial cells. In CMV-infected hCECs, upregulation of TNF-α and NF-κB was determined by WB and ICC. In hCECs, CMV infection induced apoptosis and significantly impaired cell-cell contacts, effects that were attenuated by treatment with a ROCK inhibitor. CONCLUSIONS. Aqueous TNF-α was upregulated in CMV+/PSS patients, which may have triggered corneal endothelial cell loss. Modulation of TNF-α, including its downstream Rho-ROCK signaling, could serve as a novel treatment modality for corneal endothelial cell loss in CMV+/PSS patients.

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“…In fact, it is well established the role of cysteine in alleviating intestinal inflammation and oxidative stress through the inhibition the NF-κB and the activation of the Nrf2 signaling pathways [36], which modulates the proliferation of epithelial cell. Similarly, it is well known that the activation of NF-kB pathway is involved in corneal inflammation [37], which could justify the beneficial effects of l-cysteine on corneal regeneration.…”

Section: Discussionmentioning

confidence: 97%

Oral l-Cysteine Supplementation Enhances the Long Term-Effect of Topical Basic Fibroblast Growth Factor (bFGF) in Reducing the Corneal Haze after Photorefractive Keratectomy in Myopic Patients

et al. 2020

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We aimed at evaluating the long-term effects of l-cysteine oral supplementation to basic fibroblast growth factor (bFGF) eye-drops on corneal re-epithelization and transparency in myopic patients subjected to photorefractive keratectomy (PRK). Forty patients subjected to bilateral PRK for myopia were enrolled and randomly divided into two groups receiving an additional therapy together with the standard postoperative treatment consisting in local tobramycin 0.3%, dexamethasone 0.1%, diclofenac 0.1%, and 0.2% hyaluronate. Group 1 included 20 patients (11 males and 9 females; 34.09 ± 8 years of age) receiving only bFGF eye-drops (10 μg/10 μL) four times a day for 7 days starting from the day of surgery; Group 2 included 20 patients (12 males and 8 females; 37.35 ± 11.5 years of age) who were postoperatively administered with topical basic fibroblast growth factor (bFGF; 10 μg/10 μL) four times a day for 7 days plus oral l-cysteine supplementation (500 mg/capsule) once a day for 15 days, starting 7 days before PRK. Patients were followed-up for 12 months. Clinical ophthalmologic parameters were recorded for all the 80 examined eyes. The corneal transparency was evaluated in vivo by slit lamp and confocal microscopy. The data showed that: (a) the corneal haze occurred in a smaller percentage of the patients who were postoperatively administered with topical bFGF plus oral l-cysteine supplementation (Group 2) compared to patients who received only bFGF (Group 1); (b) at 6 months of follow-up, the stromal mean image brightness of the patients belonging to Group 2 was significantly lower than that of the Group 1 (p < 0.03), and, interestingly, the difference was even more evident at 12 month from the treatment (p < 0.001). Moreover, the final mean of the spherical equivalent refraction was −0.06 ± 0.2 D in Group 1 and −0.08 ± 0.3 D in Group 2, whereas the final uncorrected distance visual acuity (UDVA) was equal or superior to 20/25 in 100% of eyes in both Group 1 and 2. Post refractive patients can benefit from the administration of l-cysteine before the surgery and in association with bFGF in the early postoperative period, showing a faster corneal re-epithelization able to prevent corneal haze in the long-term recovery.

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Rho Kinase Type 1 (ROCK1) Promotes Lipopolysaccharide-induced Inflammation in Corneal Epithelial Cells by Activating Toll-Like Receptor 4 (TLR4)-Mediated Signaling

Cited by 17 publications

References 24 publications

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

Effects of ROCK Inhibitors on Apoptosis of Corneal Endothelial Cells in CMV-Positive Posner–Schlossman Syndrome Patients

Oral l-Cysteine Supplementation Enhances the Long Term-Effect of Topical Basic Fibroblast Growth Factor (bFGF) in Reducing the Corneal Haze after Photorefractive Keratectomy in Myopic Patients

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