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Japanese scientists have discovered the chemical that induces bone marrow to produce healing cells.  From the story:

The chemical which summons stem cells from bone marrow to the site of a wound has been discovered by scientists in the UK and Japan. The study, published in Proceedings of the National Academy of Sciences, identified the distress signal – HMGB1. The authors believe it can be used to put “a megaphone in the system” to improve the treatment of injuries such as burns and leg ulcers.  Bone marrow was thought to play a role in repairing damaged skin, but the exact process was unknown. Scientists at Osaka University and King’s College London gave mice bone marrow cells that glow green – which can be tracked while moving round the body.

They then wounded the mice and some were given skin grafts. In mice without grafts, very few stem cells travelled to the wound. Those with grafts had many stem cells travelling to the wound. Professor John McGrath, from King’s College London, says grafted skin tissue has no blood vessels and therefore no oxygen. He says this environment leads to the release of HMGB1 – or what he called a ‘Save Our Skin signal’ – which results in stem cells moving to the wound. He said: “It could have a very big impact on regenerative medicine for treating people with rare genetic illnesses and more common problems such as burns and ulcers. “It could potentially revolutionise the management of wound healing.”

Source/Fonte: BBC

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PDGFRα-positive cells in bone marrow are mobilized by high mobility group box 1 (HMGB1) to regenerate injured epithelia

1. Katsuto Tamai^a,¹, 
2. Takehiko Yamazaki^a, 
3. Takenao Chino^a,
4. Masaru Ishii^b, 
5. Satoru Otsuru^a, 
6. Yasushi Kikuchi^a, 
7. Shin Iinuma^a,
8. Kotaro Saga^a, 
9. Keisuke Nimura^a, 
10. Takashi Shimbo^a, 
11. Noriko Umegaki^c,
12. Ichiro Katayama^c, 
13. Jun-ichi Miyazaki^d, 
14. Junji Takeda^e, 
15. John A. McGrath^f,
16. Jouni Uitto^g, and 
17. Yasufumi Kaneda^a,¹

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Author Affiliations

1. ^aDivision of Gene Therapy Science, and
2. Departments of ^cDermatology,
3. ^dNutrition and Physiological Chemistry, and
4. ^eEnvironmental Medicine, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan;
5. ^bLaboratory of Biological Imaging, WPI-Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan;
6. ^fSt. John's Institute of Dermatology, King's College London, Guy's Hospital, London SE1 9RT, United Kingdom; and
7. ^gDepartment of Dermatology and Cutaneous Biology, Jefferson Medical College, Philadelphia, PA 19107

Edited by Darwin J. Prockop, Texas A & M Health Science Center, Temple, TX, and approved March 18, 2011 (received for review November 10, 2010)

Abstract

The role of bone marrow cells in repairing ectodermal tissue, such as skin epidermis, is not clear. To explore this process further, this study examined a particular form of cutaneous repair, skin grafting. Grafting of full thickness wild-type mouse skin onto mice that had received a green fluorescent protein-bone marrow transplant after whole body irradiation led to an abundance of bone marrow-derived epithelial cells in follicular and interfollicular epidermis that persisted for at least 5 mo. The source of the epithelial progenitors was the nonhematopoietic, platelet-derived growth factor receptor α-positive (Lin−/PDGFRα+) bone marrow cell population. Skin grafts release high mobility group box 1 (HMGB1) in vitro and in vivo, which can mobilize the Lin−/PDGFRα+cells from bone marrow to target the engrafted skin. These data provide unique insight into how skin grafts facilitate tissue repair and identify strategies germane to regenerative medicine for skin and, perhaps, other ectodermal defects or diseases.

epidermolysis bullosa skin injury stem cells keratinocyte tissue regeneration

Footnotes

1To whom correspondence may be addressed. 

E-mail:tamai@gts.med.osaka-u.ac.jp or kaneday@gts.med.osaka-u.ac.jp.

Author contributions: K.T. designed research; K.T., T.Y., T.C., M.I., S.O., Y. Kikuchi, S.I., K.S., K.N., T.S., and N.U. performed research; J.-i.M. and J.T. contributed new reagents/analytic tools; K.T., I.K., and Y. Kaneda analyzed data; and K.T., J.A.M., J.U., and Y. Kaneda wrote the paper.

Conflict of interest statement: K.T., T.Y., and Y. Kaneda have filed patents relating to the use of HMGB1 for bone marrow cell mobilization and recruitment to damaged tissue. These individuals also hold stock in Genomix plc, a bio-tech company involved in HMGB1 translational research.

This article is a PNAS Direct Submission.

This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1016753108/-/DCSupplemental.

Freely available online through the PNAS open access option.

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