WOUND CONTRACTION

Keratinocytes and Matrix metalloproteinases: driving force of skin wound contraction?

 Coordinatore UNIVERSITAET BREMEN 

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 Nazionalità Coordinatore D codicestrano [D]
 Totale costo 1˙299˙840 €
 EC contributo 1˙299˙840 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2009-StG
 Funding Scheme ERC-SG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-12-01   -   2015-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    MEDIZINISCHE HOCHSCHULE HANNOVER

 Organization address address: Carl-Neuberg-Strasse 1
city: HANNOVER
postcode: 30625

contact info
Titolo: Mr.
Nome: Frank
Cognome: Dittrich
Email: send email
Telefono: +49 511 532 5343
Fax: +49 511 532 5203

DE (HANNOVER) beneficiary 410˙945.60
2    JACOBS UNIVERSITY BREMEN GGMBH

 Organization address address: Campus Ring 1
city: BREMEN
postcode: 28759

contact info
Titolo: Mr.
Nome: Ronald
Cognome: Kieschnick
Email: send email
Telefono: +49 421 2004515

DE (BREMEN) beneficiary 0.00
3    UNIVERSITAET BREMEN

 Organization address address: Bibliothekstrasse 1
city: BREMEN
postcode: 28359

contact info
Titolo: Dr.
Nome: Ursula
Cognome: Mirastschijski
Email: send email
Telefono: +49 175 2776807
Fax: +49 421 2184279

DE (BREMEN) hostInstitution 888˙894.44
4    UNIVERSITAET BREMEN

 Organization address address: Bibliothekstrasse 1
city: BREMEN
postcode: 28359

contact info
Titolo: Ms.
Nome: Silke
Cognome: Reinold
Email: send email
Telefono: +49 421 21860326
Fax: +49 421 2189860326

DE (BREMEN) hostInstitution 888˙894.44

Mappa


 Word cloud

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medical    molecules    scarring    unconventional    paradigm    induce    cell    surfactants    tension    keratinocytes    healing    adhesion    contraction    wounds    wound    matrix    epidermal    surface    epithelialisation    reduce    mmp   

 Obiettivo del progetto (Objective)

'Two unconventional concepts of skin contraction are presented that could change the current paradigm of wound healing. The overall objective is to clarify the underlying processes and to develop new therapies to prevent excessive scarring, ameliorate patients lives and reduce medical health care expenses. Specific emphasis lies on the role of Matrix metalloproteinases (MMP) and keratinocytes. Previous internationally acknowledged work of the PI resulted in these challenging concepts. The project will take place at the Medical School Hannover with its vast scientific infrastructure perfectly suited for this type of pioneer research. Unconventional is the concept that MMP lead to contrary cell responses. By degrading matrix molecules, MMP induce cell disassembly and migration. Only MMP-3 and -7 cleave cadherins and induce adhesion. MMP-3 deficient mice showed normal wound epithelialisation without contraction. Presumably by controlled proteolysis of intercellular molecules, cell adhesivity increases. Firm adhesion complexes provide stable anchorage sites for force generation. Selective MMP-3 inhibition would reduce contraction without impairing epithelialisation. The concept of the epithelial role in contraction differs from the paradigm and marks a beyond the state-of-art approach in wound healing. Keratinocytes at the air-liquid interphase close wounds by reepithelialisation and surface minimization. Hence, reduction of surface tension would decrease epidermal contraction. Alveolar surface tension is reduced by surfactants in preterm infants. Assuming that epidermal wounds could profit of surfactants is a high risk high gain approach of tackling hypertrophic scarring, but if successful it would revolutionize burn wound therapy.'

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