Expression of endoglin in psoriatic involved and uninvolved skin

Rulo, H. F. C.; Westphal, Johan R.; Kerkhof, P.C.M. van de; Waal, R.M.W. de; Vlijmen, I.M.J.J.; Ruiter, Dirk J.

doi:10.1016/0923-1811(95)00397-b

Cited by 25 publications

(19 citation statements)

References 19 publications

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“…Eng expression increases after dermal wound in association with inflammation (Torsney et al, 2002). In addition, Eng is overexpressed in some skin diseases such as scleroderma or psoriasis (Rulo et al, 1995;Maring et al, 2012). The purpose of this study was to assess the role of Eng in epidermal reepithelialization by studying the effect of Eng insufficiency on cutaneous healing after an excisional wound.…”

Section: Introductionmentioning

confidence: 99%

Impaired Wound Repair in Adult Endoglin Heterozygous Mice Associated with Lower NO Bioavailability

Pérez-Gómez

Jerkić

Prieto

et al. 2014

Journal of Investigative Dermatology

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Endoglin (Eng) is a transmembrane glycoprotein that is mainly expressed in endothelial cells, but it is also present in the epidermis and skin appendages. To address the role of Eng in cutaneous wound healing, we compared the kinetics of reepithelialization in Eng heterozygous null (Eng(+/-)) mice and their normal littermates (Eng(+/+)) following skin wounds. The wound area was significantly larger in Eng(+/-) than in Eng(+/+) mice from 2 to 8 days after injury; overall wound closure was delayed by 1 to 2 days. In Eng(+/-) mice, keratinocytes at the wound edges exhibited impaired proliferation but were more migratory, as shown by their elongated morphology and increased keratin 17 expression. Inhibition of nitric oxide (NO) synthesis delayed healing in Eng(+/+) but not in Eng(+/-) mice. Administration of the NO donor LA-803 accelerated wound closure in Eng(+/-) mice, with no effect on normal littermates. The acute stimulation with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced Eng expression in mouse epidermal keratinocytes in vivo and in vitro associated with hyperproliferation. Similarly, the skin of Eng(+/-) mice failed to mount a hyperplastic response to acute stimulation with TPA. These results demonstrate an important involvement of Eng in wound healing that is associated with NO bioavailability.

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Section: Introductionmentioning

confidence: 99%

Impaired Wound Repair in Adult Endoglin Heterozygous Mice Associated with Lower NO Bioavailability

Pérez-Gómez

Jerkić

Prieto

et al. 2014

Journal of Investigative Dermatology

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“…Endoglin is expressed at low levels in resting ECs, but it is highly expressed in vascular ECs at sites of active angiogenesis, during embryogenesis (80,131), and in inflamed tissues and healing wounds (163), psoriatic skin (145), inflamed synovial arthritis (155), upon vascular injury (21), and in tumor vessels (13,25,55,119). Endoglin is also overexpressed after ischemia and reperfusion in the kidney (47), hindlimbs (79), and heart (168).…”

Section: Regulation Of Endoglin Expressionmentioning

confidence: 99%

The physiological role of endoglin in the cardiovascular system

López‐Novoa

Bernabeu

2010

American Journal of Physiology-Heart and Circulatory Physiology

190

200

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Endoglin (CD105) is an integral membrane glycoprotein that serves as a coreceptor for members of the transforming growth factor-β superfamily of proteins. A major role for endoglin in regulating transforming growth factor-β-dependent vascular remodeling and angiogenesis has been postulated based on the following: 1) endoglin is the gene mutated in hereditary hemorrhagic telangiectasia type 1, a disease characterized by vascular malformations; 2) endoglin knockout mice die at midgestation because of defective angiogenesis; 3) endoglin is overexpressed in neoangiogenic vessels, during inflammation, and in solid tumors; and 4) endoglin regulates the expression and activity of endothelial nitric oxide synthase, which is involved in angiogenesis and vascular tone. Besides the predominant form of the endoglin receptor (long endoglin isoform), two additional forms of endoglin have been recently reported to play a role in the vascular pathology and homeostasis: the alternatively spliced short endoglin isoform and a soluble endoglin form that is proteolytically cleaved from membrane-bound endoglin. The purpose of this review is to underline the role that the different forms of endoglin play in regulating angiogenesis, vascular remodeling, and vascular tone, as well as to analyze the molecular and cellular mechanisms supporting these effects.

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“…In addition, increased levels of the membrane and soluble forms of endoglin have been linked to inflammatory processes, such as wound healing, atherosclerosis, psoriasis and rheumatoid arthritis (Rulo et al, 1995;Conley et al, 2000;Torsney et al, 2002;López-Novoa and Bernabeu, 2010).…”

Section: Introductionmentioning

confidence: 99%

Expression of endoglin isoforms in the myeloid lineage and their role during aging and macrophage polarization

Aristorena¹,

Blanco²,

Casas-Engel³

et al. 2014

Journal of Cell Science

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Endoglin plays a crucial role in pathophysiological processes such as hereditary hemorrhagic telangiectasia (HHT), preeclampsia and cancer. Endoglin expression is upregulated during the monocyte-tomacrophage transition, but little is known about its regulation and function in these immune cells. Two different alternatively spliced isoforms of endoglin have been reported, L-endoglin and S-endoglin. Although L-endoglin is the predominant variant, here, we found that there was an increased expression of the S-endoglin isoform during senescence of the myeloid lineage in human and murine models. We performed a stable isotope labelling of amino acids in cell culture (SILAC) analysis of both L-endoglin and S-endoglin transfectants in the human promonocytic cell line U937. Analysis of differentially expressed protein clusters allowed the identification of cellular activities affected during aging. S-endoglin expression led to decreased cellular proliferation and a decreased survival response to granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced apoptosis, as well as increased oxidative stress. Gene expression and functional studies suggested that there was a nonredundant role for each endoglin isoform in monocyte biology. In addition, we found that S-endoglin impairs the monocytic differentiation into the pro-inflammatory M1 phenotype and contributes to the compromised status of macrophage functions during aging.

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Expression of endoglin in psoriatic involved and uninvolved skin

Cited by 25 publications

References 19 publications

Impaired Wound Repair in Adult Endoglin Heterozygous Mice Associated with Lower NO Bioavailability

Impaired Wound Repair in Adult Endoglin Heterozygous Mice Associated with Lower NO Bioavailability

The physiological role of endoglin in the cardiovascular system

Expression of endoglin isoforms in the myeloid lineage and their role during aging and macrophage polarization

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