Use of porcine tumor necrosis factor receptor 1‐Ig fusion protein to prolong xenograft survival

Costa, Cristina; Bell, Natalie; Stabel, Thomas J.; Fodor, William L.

doi:10.1111/j.1399-3089.2004.00169.x

Cited by 18 publications

(26 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PAEC cells –Porcine Aortic Endothelial Cells– (gift from Dr. Cristina Costa, Institut d’Investigació Biomèdica de Bellvitge, l’Hospitalet de Llobregat, Barcelona, Spain [47]) were cultured in RPMI 1640 (Invitrogen) supplemented with 10% heat-inactivated bovine serum (Invitrogen) and endothelial mitogen (50 mg/l; Biomedical Technologies Inc.). All cell lines were incubated at 37°C in a humidified atmosphere of 5% CO 2 in air.…”

Section: Methodsmentioning

confidence: 99%

EphA2-Induced Angiogenesis in Ewing Sarcoma Cells Works through bFGF Production and Is Dependent on Caveolin-1

et al. 2013

View full text Add to dashboard Cite

Angiogenesis is the result of the combined activity of the tumor microenvironment and signaling molecules. The angiogenic switch is represented as an imbalance between pro- and anti-angiogenic factors and is a rate-limiting step in the development of tumors. Eph receptor tyrosine kinases and their membrane-anchored ligands, known as ephrins, constitute the largest receptor tyrosine kinase (RTK) subfamily and are considered a major family of pro-angiogenic RTKs. Ewing sarcoma (EWS) is a highly aggressive bone and soft tissue tumor affecting children and young adults. As other solid tumors, EWS are reliant on a functional vascular network for the delivery of nutrients and oxygen and for the removal of waste. Based on the biological roles of EphA2 in promoting angiogenesis, we explored the functional role of this receptor and its relationship with caveolin-1 (CAV1) in EWS angiogenesis. We demonstrated that lack of CAV1 results in a significant reduction in micro vascular density (MVD) on 3 different in vivo models. In vitro, this phenomenon correlated with inactivation of EphA2 receptor, lack of AKT response and downregulation of bFGF. We also demonstrated that secreted bFGF from EWS cells acted as chemoattractant for endothelial cells. Furthermore, interaction between EphA2 and CAV1 was necessary for the right localization and signaling of the receptor to produce bFGF through AKT and promote migration of endothelial cells. Finally, introduction of a dominant-negative form of EphA2 into EWS cells mostly reproduced the effects occurred by CAV1 silencing, strongly suggesting that the axis EphA2-CAV1 participates in the promotion of endothelial cell migration toward the tumors favoring EWS angiogenesis.

show abstract

Section: Methodsmentioning

confidence: 99%

EphA2-Induced Angiogenesis in Ewing Sarcoma Cells Works through bFGF Production and Is Dependent on Caveolin-1

et al. 2013

View full text Add to dashboard Cite

show abstract

“…This or a similar pharmaceutical approach to improve organ preservation coupled with the transplantation of GTKO hearts expressing one or more hCRPs with possible antibody depletion prior to transplant may be effective to alleviate early antibody‐mediated graft injury and reduce the frequency of fatal PCXD. Prophylactic use of anti‐cytokine reagents, such as etanercept (Enbrel) to block TNF‐α or anakinra (Kineret) to block IL‐1 may be used to limit perioperative inflammation of vascular endothelial cells and may further reduce the potential for PCXD. Donor hearts expressing elevated levels of CD39 are resistant to ischemia–reperfusion injury and may represent a non‐pharmaceutical solution to modulate PCXD .…”

Section: Future Strategiesmentioning

confidence: 99%

Histopathologic insights into the mechanism of anti‐non‐Gal antibody‐mediated pig cardiac xenograft rejection

Byrne

Azimzadeh

Ezzelarab

et al. 2013

Xenotransplantation

View full text Add to dashboard Cite

The histopathology of cardiac xenograft rejection has evolved over the last 20 years with the development of new modalities for limiting antibody-mediated injury, advancing regimens for immune suppression, and an ever-widening variety of new donor genetics. These new technologies have helped us progress from what was once an overwhelming anti-Gal-mediated hyperacute rejection to a more protracted anti-Gal-mediated vascular rejection, to what is now a more complex manifestation of nonGal humoral rejection and coagulation dysregulation. This review summarizes the changing histopathology of Gal and nonGal-mediated cardiac xenograft rejection and discusses the contributions of immune-mediated injury, species-specific immune-independent factors, transplant and therapeutic procedures, and donor genetics to the overall mechanism(s) of cardiac xenograft rejection.

show abstract

“…To further investigate the mechanism of the rejection of xenografted cells in vivo, cell transplant studies were also performed [28,29]. Stable PEC transfectants of either human decoy Fas or membrane-bound human FasL were established by Death receptor remodeling improves islet xenograft survival lipofection.…”

Section: Cell Transplant Studiesmentioning

confidence: 99%

Prolonged survival of pig islets xenograft by adenovirus‐mediated expression of either the membrane‐bound human FasL or the human decoy Fas antigen gene

Kikuchi

Tanemura

Ito

et al. 2008

Xenotransplantation

View full text Add to dashboard Cite

show abstract

Use of porcine tumor necrosis factor receptor 1‐Ig fusion protein to prolong xenograft survival

Abstract: Incorporation of strategies that block TNF may prove useful in the development of xenografts resistant to delayed rejection.

Cited by 18 publications

References 57 publications

EphA2-Induced Angiogenesis in Ewing Sarcoma Cells Works through bFGF Production and Is Dependent on Caveolin-1

EphA2-Induced Angiogenesis in Ewing Sarcoma Cells Works through bFGF Production and Is Dependent on Caveolin-1

Histopathologic insights into the mechanism of anti‐non‐Gal antibody‐mediated pig cardiac xenograft rejection

Prolonged survival of pig islets xenograft by adenovirus‐mediated expression of either the membrane‐bound human FasL or the human decoy Fas antigen gene

Contact Info

Product

Resources

About