Implication of Hsc70, PDI and integrin αvβ3 involvement during entry of the murine rotavirus ECwt into small-intestinal villi of suckling mice

Santana, Ana Y.; Guerrero, C.; Acosta, Orlando

doi:10.1007/s00705-013-1626-6

Cited by 12 publications

(15 citation statements)

References 46 publications

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“…Similarly, thiol groups are generated in the outer capsid proteins after TLPs contact the cell surface, suggesting that PDI or other related thioredoxins are able to reduce disulfide bonds in viral proteins (Rivera M, Guerrero CA, Acosta O, manuscript in preparation). Studies characterizing potential cell surface receptors for rotavirus infection of small intestinal villus cells from mice showed that raft-associated Hsc70, PDI and integrin β3 played an important role in the rotavirus entry process as previously shown for MA104 cells [127] . It has been reported that integrin subunit β3 and integrin α2β1 are present on the cell surface of murine and human enterocytes [157,158] , and that rotavirus-susceptible MA104, COS7 and Caco-2 cells also contain cell surface receptors including αvβ3 and Hsc70 [113,128] .…”

Section: Dlp-tlp Inter-conversionsupporting

confidence: 56%

“…It has been reported that integrin subunit β3 and integrin α2β1 are present on the cell surface of murine and human enterocytes [157,158] , and that rotavirus-susceptible MA104, COS7 and Caco-2 cells also contain cell surface receptors including αvβ3 and Hsc70 [113,128] . The colocalization of PDI, integrin β3, Hsc70 and rotavirus particles in lipid microdomains (rafts) from MA104 and intestinal villus cells [12,127] suggest that PDI reducing function at cell surface can activate either integrins or VP7 to interact each other during entry [94] . The role of thiol-disulfide exchange during rotavirus infection is well documented, but the detailed processes of this implication still remain incompletely elucidated.…”

Section: Dlp-tlp Inter-conversionmentioning

confidence: 99%

“…PDI, Hsc70 and integrin αvβ3 have been found to interact in lipid microdomains ("rafts") [12,127] , which have been proposed as being essential platforms facilitating efficient interaction between virus particles and cellular receptors [96,128] . On the other hand, some reports have indicated that PDI forms complexes with integrins α2β1 and αvβ3 [129,130] that have been identified as cell surface rotavirus receptors in MA104 cells.…”

mentioning

confidence: 99%

“…However, studies using intestinal cell lines showed that rotavirus infection up-regulated the expression of integrins α2β1 and β2, whereas down-regulated that of integrins αvβ3, αvβ5, and α5β1 [136] . It would be interesting to examine whether cell surface PDI activates integrin β3 to facilitate rotavirus infection since PDI expression has been up-regulated by rotavirus infection [127] . It has been found that dengue virus infection increases cell surface PDI expression for activating integrins β1 and β3 and facilitating virus entry into epithelial cells [83] .…”

mentioning

confidence: 99%

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Inflammatory and oxidative stress in rotavirus infection

Guerrero¹,

Acosta²

2016

WJV

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Rotaviruses are the single leading cause of life-threatening diarrhea affecting children under 5 years of age. Rotavirus entry into the host cell seems to occur by sequential interactions between virion proteins and various cell surface molecules. The entry mechanisms seem to involve the contribution of cellular molecules having binding, chaperoning and oxido-reducing activities. It appears to be that the receptor usage and tropism of rotaviruses is determined by the species, cell line and rotavirus strain. Rotaviruses have evolved functions which can antagonize the host innate immune response, whereas are able to induce endoplasmic reticulum (ER) stress, oxidative stress and inflammatory signaling. A networking between ER stress, inflammation and oxidative stress is suggested, in which release of calcium from the ER increases the generation of mitochondrial reactive oxygen species (ROS) leading to toxic accumulation of ROS within ER and mitochondria. Sustained ER stress potentially stimulates inflammatory response through unfolded protein response pathways. However, the detailed characterization of the molecular mechanisms underpinning these rotavirus-induced stressful conditions is still lacking. The signaling events triggered by host recognition of virusassociated molecular patterns offers an opportunity for the development of novel therapeutic strategies aimed at interfering with rotavirus infection. The use of N-acetylcysteine, non-steroidal anti-inflammatory drugs and PPARγ agonists to inhibit rotavirus infection opens a new way for treating the rotavirus-induced diarrhea and complementing vaccines. Core tip: Rotavirus entry into the host cell requires cell surface molecules providing binding, chaperoning and oxido-reducing functions. Sialic acid/integrin α2β1, heat shock cognate protein 70 and protein disulfide isomerase (PDI) seem to perform these functions. Recently, the cell surface oxido-reduction activity based at least on PDI has been highlighted as a potential determinant of the conformational changes that are required by viral structural proteins in order to facilitate virus entry. The rotavirus-induced oxidative stress and inflammatory signaling is an attractive target for therapeutic intervention as antioxidant and anti-inflammatory treatment has Submit a

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Section: Dlp-tlp Inter-conversionsupporting

confidence: 56%

Section: Dlp-tlp Inter-conversionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Inflammatory and oxidative stress in rotavirus infection

Guerrero¹,

Acosta²

2016

WJV

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“…Another Hsp related to S. aureus internalization in NPPCs is Hsc70. This protein is associated with viral infections by acting as a receptor for human T-cell lymphotropic virus type 1 (HTLV-1) [64] or rotaviruses [65, 66]. Hsc70 interacts with S. aureus hydrolases such as autolysin (Atl) during the bacterial internalization process.…”

Section: Heat Shock Proteinsmentioning

confidence: 99%

Nonprofessional Phagocytic Cell Receptors Involved inStaphylococcus aureusInternalization

Alva-Murillo

López‐Meza

Ochoa‐Zarzosa

2014

BioMed Research International

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Staphylococcus aureus is a successful human and animal pathogen. The majority of infections caused by this pathogen are life threatening, primarily because S. aureus has developed multiple evasion strategies, possesses intracellular persistence for long periods, and targets the skin and soft tissues. Therefore, it is very important to understand the mechanisms employed by S. aureus to colonize and proliferate in these cells. The aim of this review is to describe the recent discoveries concerning the host receptors of nonprofessional phagocytes involved in S. aureus internalization. Most of the knowledge related to the interaction of S. aureus with its host cells has been described in professional phagocytic cells such as macrophages. Here, we showed that in nonprofessional phagocytes the α5β1 integrin host receptor, chaperons, and the scavenger receptor CD36 are the main receptors employed during S. aureus internalization. The characterization and identification of new bacterial effectors and the host cell receptors involved will undoubtedly lead to new discoveries with beneficial purposes.

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