Calreticulin induced endothelial ICAM-1 up-regulation associated with tristetraprolin expression alteration through PI3K/Akt/eNOS/p38 MAPK signaling pathway in rheumatoid arthritis

Liu, Yixin; Wei, Wei; Hong, Chengcheng; Wang, Yan; Sun, Xin; Ma, Jun; Zheng, Fang

doi:10.1016/j.molimm.2019.01.005

Cited by 17 publications

(9 citation statements)

References 35 publications

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“…et al; Mesaeli et al) la han ubicado en matriz extracelular dónde podría tener diferentes funciones. Liu et al (2019) correlacionaron los niveles de CRT con ICAM-1 y VCAM-1 en el suero y líquido sinovial de pacientes con artritis reumatoide, encontrando una elevada co-expresión de CRT con ICAM-1 en las áreas perivasculares del líquido sinovial y una elevada correlación de CRT y VCAM-1 asociada principalmente a la capa de revestimiento sinovial. Además, identificaron, en un modelo de células endoteliales de venas umbilicales humanas, una elevada expresión de ICAM-1 y un aumento en los niveles de fosforilación de Akt y la óxido nítrico sintasa endotelial (eNOS) en presencia de CRT extracelular.…”

Section: Resultsunclassified

Análisis de Expresión de Calreticulina en Vena Safena Parva

et al. 2020

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RESUMEN: La proteína chaperona Calreticulina (CRT), ha sido identificada en retículo endoplásmico (RE) y últimamente en la matriz extracelular (MEC) de predentina y arterias, atribuyéndole diferentes funciones extracelulares entre las que destacan la adhesión celular, regulación de la MEC y prevención en la formación de trombos. El objetivo del estudio fue identificar la presencia de CRT en MEC de vena safena parva. Se extrajo una muestra de vena safena parva de un espécimen masculino y luego fue procesada por medios histológicos e inmunohistoquímicos para identificar su presencia. Mediante técnicas de inmunohistoquímica se pudo evidenciar la presencia de CRT en la MEC de la adventicia de vena safena parva. La presencia de CRT en MEC de safena parva orienta a que CRT tienen funciones de tipo extracelular en esta localización, pero es necesario realizar estudios más precisos para dilucidar sus principales funciones en la zona.

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Section: Resultsunclassified

Análisis de Expresión de Calreticulina en Vena Safena Parva

et al. 2020

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“…It has been reported that RBPs regulate the function of ECs by regulating mRNA stability. For example, in the human umbilical vein ECs (HUVECs) in rheumatoid arthritis model, bonding of RBP TTP and intercellular cell adhesion molecule-1 (ICAM-1) mRNA 3′UTR decreases the stability of ICAM-1, reduces the expression of ICAM-1 in HUVECs, and participates in the inhibition of inflammatory response of rheumatoid arthritis [ 47 ]. In HUVECs treated with high glucose, bonding of HuR and Sirtuin 1 (SIRT1) mRNA increases the stability of SIRT1 mRNA, thus inhibits E-selectin release and the activation of ECs induced by inflammation and hyperglycemia [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Pseudogene ACTBP2 increases blood–brain barrier permeability by promoting KHDRBS2 transcription through recruitment of KMT2D/WDR5 in Aβ1–42 microenvironment

Liu

Zhao

et al. 2021

Cell Death Discov.

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The blood–brain barrier (BBB) has a vital role in maintaining the homeostasis of the central nervous system (CNS). Changes in the structure and function of BBB can accelerate Alzheimer’s disease (AD) development. β-Amyloid (Aβ) deposition is the major pathological event of AD. We elucidated the function and possible molecular mechanisms of the effect of pseudogene ACTBP2 on the permeability of BBB in Aβ1–42 microenvironment. BBB model treated with Aβ1–42 for 48 h were used to simulate Aβ-mediated BBB dysfunction in AD. We proved that pseudogene ACTBP2, RNA-binding protein KHDRBS2, and transcription factor HEY2 are highly expressed in ECs that were obtained in a BBB model in vitro in Aβ1–42 microenvironment. In Aβ1–42-incubated ECs, ACTBP2 recruits methyltransferases KMT2D and WDR5, binds to KHDRBS2 promoter, and promotes KHDRBS2 transcription. The interaction of KHDRBS2 with the 3′UTR of HEY2 mRNA increases the stability of HEY2 and promotes its expression. HEY2 increases BBB permeability in Aβ1–42 microenvironment by transcriptionally inhibiting the expression of ZO-1, occludin, and claudin-5. We confirmed that knocking down of Khdrbs2 or Hey2 increased the expression levels of ZO-1, occludin, and claudin-5 in APP/PS1 mice brain microvessels. ACTBP2/KHDRBS2/HEY2 axis has a crucial role in the regulation of BBB permeability in Aβ1–42 microenvironment, which may provide a novel target for the therapy of AD.

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“…Previous research has reported that calreticulin active p38 MAPK signaling through increasing phosphorylation of NOS3, and finally promote inflammation in rheumatoid arthritis. 34 In type 2 diabetes mellitus and trauma-hemorrhage, it was reported that p38 MAPK activation enhanced NOS phosphorylation. 35,36 However, the interaction between NOS3 and MAPK signaling in tumor cells has not been reported.…”

Section: Bufalin Suppresses Gcpd Through Targeting Nos3 In Vivomentioning

confidence: 99%

Bufalin inhibits peritoneal dissemination of gastric cancer through endothelial nitric oxide synthase‐mitogen‐activated protein kinases signaling pathway

et al. 2021

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Peritoneal dissemination threatens the survival of patients with gastric cancer (GC).Bufalin is an extract of traditional Chinese medicine, which has been proved to have anticancer effect. The target of bufalin in suppressing gastric cancer peritoneal dissemination (GCPD) and the underlying mechanism are still unclear. In this research, GC cell line MGC-803 and high-potential peritoneal dissemination cell line MKN-45P were treated with bufalin or L-NAME. Malignant biological behavior and protein level of GC cell lines were detected with MTT, wound healing, transwell, adhesion, and western blotting. Bioinformatics analysis and patient tissues were used to verify the role of endothelial nitric oxide synthase (NOS3) in GC. Mice model was used to assess the effect of bufalin and role of NOS3 in vivo. We found that bufalin inhibited the proliferation, invasion, and migration in GC cell lines. NOS3, which was an independent prognostic factor of GC patients, was predicted to be a potential target of bufalin. Further experiments proved that bufalin reduced the phosphorylation of NOS3, thereby inhibiting the mitogen-activated protein kinase (MAPK) signaling pathway, and ultimately suppressed GCPD by inhibiting EMT process. In conclusion, NOS3 was a potential therapeutic target and prognostic biomarker of GC. Bufalin could suppress GCPD through NOS3-MAPK signaling pathway, which provided more evidence support for intraperitoneal perfusion of bufalin to treat GCPD.

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Calreticulin induced endothelial ICAM-1 up-regulation associated with tristetraprolin expression alteration through PI3K/Akt/eNOS/p38 MAPK signaling pathway in rheumatoid arthritis

Cited by 17 publications

References 35 publications

Análisis de Expresión de Calreticulina en Vena Safena Parva

Análisis de Expresión de Calreticulina en Vena Safena Parva

Pseudogene ACTBP2 increases blood–brain barrier permeability by promoting KHDRBS2 transcription through recruitment of KMT2D/WDR5 in Aβ1–42 microenvironment

Bufalin inhibits peritoneal dissemination of gastric cancer through endothelial nitric oxide synthase‐mitogen‐activated protein kinases signaling pathway

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