糖尿病和濕疹（eczema）表面上看來是完全無關(guān)的兩種疾病,，不過美國加州大學(xué)圣地亞哥分校的生物學(xué)家近日發(fā)現(xiàn),，這二者之間存在著一個(gè)至關(guān)重要的生物化學(xué)聯(lián)系。
圣地亞哥分校生物學(xué)家Colin Jamora和同事報(bào)告說,，他們發(fā)現(xiàn)先前被認(rèn)為只與細(xì)胞死亡有關(guān)的蛋白caspase 8,，在實(shí)驗(yàn)小鼠的傷口愈合方面發(fā)揮著關(guān)鍵性的作用。引人注意的是,，caspase 8在濕疹患者體內(nèi)表達(dá)不足,，而在糖尿病患者體內(nèi)則過度表達(dá)。相關(guān)論文將發(fā)表在3月26日的《自然》（Nature）雜志上,。
研究人員表示,，他們的發(fā)現(xiàn)可能解釋了為什么糖尿病患者在面對(duì)微小傷口時(shí),，會(huì)缺乏正常的傷應(yīng)，并因此遭受嚴(yán)重的并發(fā)癥,；以及為什么濕疹患者的皮膚會(huì)出現(xiàn)慢性炎癥,，從而危及它的保護(hù)功能。
Jamora說：“caspase 8的缺失會(huì)刺激發(fā)炎,，產(chǎn)生大量細(xì)胞阻止細(xì)菌感染傷口,。它還會(huì)刺激一些干細(xì)胞的產(chǎn)生，這些干細(xì)胞提供一些材料幫助愈合傷口,。這很重要,，因?yàn)樵趥诘淖畛蹼A段，皮膚的保護(hù)層被破壞,，內(nèi)在機(jī)體均暴露于細(xì)菌和環(huán)境毒素,。”
Jamora目前和同事正在研究糖尿病的實(shí)驗(yàn)鼠模型，以確定人工阻尼caspase 8的產(chǎn)生是否會(huì)恢復(fù)它們愈合傷口的能力,。同時(shí),，Jamora說：“我們也在用caspase-8敲除小鼠作為模型系統(tǒng)來研究濕疹，以確定各種病理要素,，并借此揭示該病新的靶標(biāo),，為全世界患有該病的10%至20%的兒童造福。”（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 8 February 2009 | doi:10.1038/nature07687
Dynamic expression of epidermal caspase 8 simulates a wound healing response
Pedro Lee1, Dai-Jen Lee1, Carol Chan1, Shih-Wei Chen1, Irene Ch'en2 & Colin Jamora1,3
1 Section of Cell and Developmental Biology, Division of Biological Sciences, Natural Science Building, Room 6311, 9500 Gilman Drive, MC 0380
2 Section of Molecular Biology, Division of Biological Sciences, Natural Science Building, Room 5116, 9500 Gilman Drive, MC 0377
3 Department of Medicine (Dermatology), Natural Science Building, Room 6113, 9500 Gilman Drive, MC 0380, La Jolla, California 92093, USA
Correspondence to: Colin Jamora1,3 Correspondence and requests for materials should be addressed to C.J.
Tissue homeostasis and regeneration are regulated by an intricate balance of seemingly competing processes—proliferation versus differentiation, and cell death versus survival1. Here we demonstrate that the loss of epidermal caspase 8, an important mediator of apoptosis2, recapitulates several phases of a wound healing response in the mouse. The epidermal hyperplasia in the caspase 8 null skin is the culmination of signals exchanged between epidermal keratinocytes, dermal fibroblasts and leukocytic cells. This reciprocal interaction is initiated by the paracrine signalling of interleukin 1 (IL1), which activates both skin stem cell proliferation and cutaneous inflammation. The non-canonical secretion of IL1 is induced by a p38-MAPK-mediated upregulation of NALP3 (also known as NLRP3), leading to inflammasome assembly and caspase 1 activation. Notably, the increased proliferation of basal keratinocytes is counterbalanced by the growth arrest of suprabasal keratinocytes in the stratified epidermis by IL1-dependent NFB signalling. Altogether, our findings illustrate how the loss of caspase 8 can affect more than programmed cell death to alter the local microenvironment and elicit processes common to wound repair and many neoplastic skin disorders.
