CD105 is important for angiogenesis: evidence and potential applications

Duff, Sarah; Li, Chenggang; Garland, John M.; Kumar, Shant

doi:10.1096/fj.02-0634rev

Cited by 481 publications

(429 citation statements)

References 67 publications

Supporting

Mentioning

394

Contrasting

Unclassified

Order By: Relevance

“…To test whether cNGR specifically binds to angiogenic endothelial cells, experiments using anti-CD105-FITC 13 were performed, both in healthy (nϭ3) and infarcted (nϭ4) tissue. In noninfarcted tissue of both MI and healthy mice CD105 had low expression in the microvascular endothelium illustrated by co-localization with CD31 ( Figure 5E).…”

Section: Tplsm: Cellular Localization Of Cngr After In Vivo Injectionmentioning

confidence: 99%

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

Buehler¹,

Zandvoort²,

Stelt³

et al. 2006

ATVB

View full text Add to dashboard Cite

Objective-Previously, the peptide sequence cNGR has been shown to home specifically to CD13/APN (aminopeptidase N) on tumor endothelium. Here, we investigated the feasibility of selective imaging of cardiac angiogenesis using the cNGR-CD13/APN system. Methods and Results-CD13/APN induction and cNGR homing were studied in the murine myocardial infarction (MI) model. By real-time polymerase chain reaction (PCR) at 7 days after MI, CD13/APN expression was 10-to 20-fold higher in the angiogenic infarct border zone and the MI area than in non-MI areas. In vivo fluorescence microscopy confirmed specific homing of fluorophore-tagged cNGR to the border zone and MI territory at 4 and 7 days after MI with a local advantage of 2.3, but not at 1 or 14 days after MI. Tissue residence half-life was 9.1Ϯ0.3 hours, whereas the half-life in plasma was 15.4Ϯ3.4 minutes. Pulse chase experiments confirmed reversible binding of cNGR in the infarct area. Fluorescent labeled cNGR conjugates or antibodies were injected in vivo, and their distribution was studied ex vivo by 2-photon laser scanning microscopy (TPLSM). cNGR co-localized exclusively with CD13/APN and the endothelial marker CD31 on vessels. Conclusions-In cardiac angiogenesis endothelial CD13/APN is upregulated. It can be targeted specifically with cNGR conjugates. In the heart cNGR binds its endothelial target only in angiogenic areas.

show abstract

Section: Tplsm: Cellular Localization Of Cngr After In Vivo Injectionmentioning

confidence: 99%

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

Buehler¹,

Zandvoort²,

Stelt³

et al. 2006

ATVB

View full text Add to dashboard Cite

show abstract

“…Endothelial cells of blood vessels are the main source of CD105 (Duff et al, 2003). Other cells including vascular smooth muscle cells, fibroblasts, macrophages, can also express CD105 to a lesser extent (Zijlmans et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Expression of Ki67 and CD105 as Proliferation and Angiogenesis Markers in Salivary Gland Tumors

Andisheh-Tadbir¹,

Pardis²,

Ashkavandi³

et al. 2012

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Objective: To investigate the association between CD105 and tumor cell proliferation in salivary gland tumors. Methods: In this study, 59 samples of salivary tumors from Khalili Hospital archive, including 20 cases of pleomorphic adenoma (PA), 20 cases of mucoepidermoid carcinoma (MEC) and 19 cases of adenoid cystic carcinoma, as well as 10 cases of normal salivary gland tissue, were reviewed by immunohistochemistry (IHC) for CD105 and Ki67 staining. Results: CD105 positive vessels were absent in normal salivary gland tissue in the vicinity of tumors (51.6% of all tumors were positive). There was a statistically significant difference in frequency of CD105 staining between PA and malignant tumors and between four groups of different lesions (p<0.000) being highest in MEC. Intratumoral microvessel density was also elevated in malignant neoplasms (2.61±3.1) as compared to PA (0.46±0.6). Normal salivary glands did not express Ki67. There was a statistically significant difference in frequency and percentage of Ki67 immunoreactivity in malignant neoplasms (86.5% and 10.7±10.8 respectively) compared to PA (50% and 0.78±0.2) and among the four groups values were highest in MEC (p<0.000). Conclusion: n this study, it was observed a higher rate of angiogenesis and cellular proliferation was noted in malignant tumors compared to benign tumors, but no correlation was observed between these two markers.

show abstract

“…Several tumor cells also express endoglin, including pre-B cell and monocytic leukemia (Quackenbush and Letarte, 1985;Haruta and Seon, 1986;Lastres et al, 1992;Zhang et al, 1996), choriocarcinoma (Letamendia et al, 1998a), ovarian carcinoma (Jindal et al, 1995), melanoma (Altomonte et al, 1996), prostate cancer (Liu et al, 2002) and basal and squamous cell carcinomas (Quintanilla et al, 2003). The presence of endoglin in both cells and vasculature of tumors has stimulated studies on the role of endoglin in cancer Takahashi et al, 2001;Duff et al, 2003). In this respect, recent reports suggest that elevated plasma levels of endoglin in patients with colorectal cancer or breast carcinoma correlate with poor prognosis Duff et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Characterization of murine S-endoglin isoform and its effects on tumor development

et al. 2005

View full text Add to dashboard Cite

Endoglin is a transmembrane glycoprotein that acts as an auxiliary receptor for transforming growth factor-b (TGF-b) and modulates cellular responses to this pleiotropic cytokine. Endoglin is strongly expressed in endothelial cells, where it appears to exert a crucial role in vascular development and angiogenesis. Two endoglin isoforms (L and S), differing in their cytoplasmic domains, have been previously characterized in human tissues. We now demonstrate the existence of similar L-and Sendoglin variants in murine tissues with 47 and 35 amino acids, respectively, in their cytoplasmic tail. RT-PCR analysis showed that L is the predominant endoglin isoform expressed in mouse tissues, although S-endoglin mRNA is significantly expressed in liver and lung, as well as in endothelial cell lines. Furthermore, a protein of size equivalent to recombinant S-endoglin expressed in mammalian cells was detected in mouse endothelial cells by Western blot analysis. L-and S-endoglin isoforms can form disulfide-linked heterodimers, as demonstrated by cotransfection of L-and S-endoglin constructs. To address the role of S-endoglin in vivo, an S-Eng þ transgenic mouse model that targets S-endoglin expression to the endothelium was generated. The lethal phenotype of endoglin-null (Eng À/À ) mice was not rescued by breeding S-Eng þ transgenic mice into the endoglin-null background. S-Eng þ mice exhibited reduced tumor growth and neovascularization after transplantation of Lewis lung carcinoma cells. In addition, S-Eng þ mice showed a drastic inhibition of benign papilloma formation when subjected to two-stage chemical skin carcinogenesis. These results point to S-endoglin as an antiangiogenic molecule, in contrast to L-endoglin which is proangiogenic.

show abstract

CD105 is important for angiogenesis: evidence and potential applications

Cited by 481 publications

References 67 publications

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

Expression of Ki67 and CD105 as Proliferation and Angiogenesis Markers in Salivary Gland Tumors

Characterization of murine S-endoglin isoform and its effects on tumor development

Contact Info

Product

Resources

About