LymphedemaV1, PubMed, Checkpoint, bibRecord, 002272

Temporal and spatial patterns of endogenous danger signal expression after wound healing and in response to lymphedema.

Identifieur interne : 002272 ( PubMed/Checkpoint ); précédent : 002271; suivant : 002273

Temporal and spatial patterns of endogenous danger signal expression after wound healing and in response to lymphedema.

Auteurs : Jamie C. Zampell [États-Unis] ; Alan Yan ; Tomer Avraham ; Victor Andrade ; Stephanie Malliaris ; Seth Aschen ; Stanley G. Rockson ; Babak J. Mehrara

Source :

American journal of physiology. Cell physiology [ 1522-1563 ] ; 2011.

RBID : pubmed:21248077

Descripteurs français

English descriptors

KwdEn :
- Animals, Chronic Disease, Endothelial Cells (physiology), Female, HMGB1 Protein (biosynthesis), HMGB1 Protein (physiology), HSP70 Heat-Shock Proteins (biosynthesis), HSP70 Heat-Shock Proteins (physiology), Humans, Inflammation (physiopathology), Lymphatic System (pathology), Lymphatic System (physiopathology), Lymphedema (pathology), Lymphedema (physiopathology), Mice, Mice, Inbred C57BL, NF-kappa B (biosynthesis), NF-kappa B (physiology), Peritonitis (pathology), Peritonitis (physiopathology), Signal Transduction (physiology), Up-Regulation (physiology), Wound Healing (physiology).
MESH :
- chemical , biosynthesis : HMGB1 Protein, HSP70 Heat-Shock Proteins, NF-kappa B.
- pathology : Lymphatic System, Lymphedema, Peritonitis.
- physiology : Endothelial Cells, HMGB1 Protein, HSP70 Heat-Shock Proteins, NF-kappa B, Signal Transduction, Up-Regulation, Wound Healing.
- physiopathology : Inflammation, Lymphatic System, Lymphedema, Peritonitis.
- Animals, Chronic Disease, Female, Humans, Mice, Mice, Inbred C57BL.

Abstract

While acute tissue injury potently induces endogenous danger signal expression, the role of these molecules in chronic wound healing and lymphedema is undefined. The purpose of this study was to determine the spatial and temporal expression patterns of the endogenous danger signals high-mobility group box 1 (HMGB1) and heat shock protein (HSP)70 during wound healing and chronic lymphatic fluid stasis. In a surgical mouse tail model of tissue injury and lymphedema, HMGB1 and HSP70 expression occurred along a spatial gradient relative to the site of injury, with peak expression at the wound and greater than twofold reduced expression within 5 mm (P < 0.05). Expression primarily occurred in cells native to injured tissue. In particular, HMGB1 was highly expressed by lymphatic endothelial cells (>40% positivity; twofold increase in chronic inflammation, P < 0.001). We found similar findings using a peritoneal inflammation model. Interestingly, upregulation of HMGB1 (2.2-fold), HSP70 (1.4-fold), and nuclear factor (NF)-κβ activation persisted at least 6 wk postoperatively only in lymphedematous tissues. Similarly, we found upregulation of endogenous danger signals in soft tissue of the arm after axillary lymphadenectomy in a mouse model and in matched biopsy samples obtained from patients with secondary lymphedema comparing normal to lymphedematous arms (2.4-fold increased HMGB1, 1.9-fold increased HSP70; P < 0.01). Finally, HMGB1 blockade significantly reduced inflammatory lymphangiogenesis within inflamed draining lymph nodes (35% reduction, P < 0.01). In conclusion, HMGB1 and HSP70 are expressed along spatial gradients and upregulated in chronic lymphatic fluid stasis. Furthermore, acute expression of endogenous danger signals may play a role in inflammatory lymphangiogenesis.

DOI: 10.1152/ajpcell.00378.2010
PubMed: 21248077

Affiliations:

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Le document en format XML

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<term>Chronic Disease</term>
<term>Endothelial Cells (physiology)</term>
<term>Female</term>
<term>HMGB1 Protein (biosynthesis)</term>
<term>HMGB1 Protein (physiology)</term>
<term>HSP70 Heat-Shock Proteins (biosynthesis)</term>
<term>HSP70 Heat-Shock Proteins (physiology)</term>
<term>Humans</term>
<term>Inflammation (physiopathology)</term>
<term>Lymphatic System (pathology)</term>
<term>Lymphatic System (physiopathology)</term>
<term>Lymphedema (pathology)</term>
<term>Lymphedema (physiopathology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>NF-kappa B (biosynthesis)</term>
<term>NF-kappa B (physiology)</term>
<term>Peritonitis (pathology)</term>
<term>Peritonitis (physiopathology)</term>
<term>Signal Transduction (physiology)</term>
<term>Up-Regulation (physiology)</term>
<term>Wound Healing (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Cellules endothéliales (physiologie)</term>
<term>Cicatrisation de plaie (physiologie)</term>
<term>Facteur de transcription NF-kappa B (biosynthèse)</term>
<term>Facteur de transcription NF-kappa B (physiologie)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Inflammation (physiopathologie)</term>
<term>Lymphoedème (anatomopathologie)</term>
<term>Lymphoedème (physiopathologie)</term>
<term>Maladie chronique</term>
<term>Protéine HMGB1 (biosynthèse)</term>
<term>Protéine HMGB1 (physiologie)</term>
<term>Protéines du choc thermique HSP70 (biosynthèse)</term>
<term>Protéines du choc thermique HSP70 (physiologie)</term>
<term>Péritonite (anatomopathologie)</term>
<term>Péritonite (physiopathologie)</term>
<term>Régulation positive (physiologie)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Système lymphatique (anatomopathologie)</term>
<term>Système lymphatique (physiopathologie)</term>
<term>Transduction du signal (physiologie)</term>
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<term>Péritonite</term>
<term>Système lymphatique</term>
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<term>Protéine HMGB1</term>
<term>Protéines du choc thermique HSP70</term>
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<term>Lymphedema</term>
<term>Peritonitis</term>
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<term>Cicatrisation de plaie</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Protéine HMGB1</term>
<term>Protéines du choc thermique HSP70</term>
<term>Régulation positive</term>
<term>Transduction du signal</term>
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<term>HMGB1 Protein</term>
<term>HSP70 Heat-Shock Proteins</term>
<term>NF-kappa B</term>
<term>Signal Transduction</term>
<term>Up-Regulation</term>
<term>Wound Healing</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Inflammation</term>
<term>Lymphoedème</term>
<term>Péritonite</term>
<term>Système lymphatique</term>
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<term>Lymphedema</term>
<term>Peritonitis</term>
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<term>Chronic Disease</term>
<term>Female</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Maladie chronique</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">While acute tissue injury potently induces endogenous danger signal expression, the role of these molecules in chronic wound healing and lymphedema is undefined. The purpose of this study was to determine the spatial and temporal expression patterns of the endogenous danger signals high-mobility group box 1 (HMGB1) and heat shock protein (HSP)70 during wound healing and chronic lymphatic fluid stasis. In a surgical mouse tail model of tissue injury and lymphedema, HMGB1 and HSP70 expression occurred along a spatial gradient relative to the site of injury, with peak expression at the wound and greater than twofold reduced expression within 5 mm (P < 0.05). Expression primarily occurred in cells native to injured tissue. In particular, HMGB1 was highly expressed by lymphatic endothelial cells (>40% positivity; twofold increase in chronic inflammation, P < 0.001). We found similar findings using a peritoneal inflammation model. Interestingly, upregulation of HMGB1 (2.2-fold), HSP70 (1.4-fold), and nuclear factor (NF)-κβ activation persisted at least 6 wk postoperatively only in lymphedematous tissues. Similarly, we found upregulation of endogenous danger signals in soft tissue of the arm after axillary lymphadenectomy in a mouse model and in matched biopsy samples obtained from patients with secondary lymphedema comparing normal to lymphedematous arms (2.4-fold increased HMGB1, 1.9-fold increased HSP70; P < 0.01). Finally, HMGB1 blockade significantly reduced inflammatory lymphangiogenesis within inflamed draining lymph nodes (35% reduction, P < 0.01). In conclusion, HMGB1 and HSP70 are expressed along spatial gradients and upregulated in chronic lymphatic fluid stasis. Furthermore, acute expression of endogenous danger signals may play a role in inflammatory lymphangiogenesis.</div>
</front>
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<Abstract><AbstractText>While acute tissue injury potently induces endogenous danger signal expression, the role of these molecules in chronic wound healing and lymphedema is undefined. The purpose of this study was to determine the spatial and temporal expression patterns of the endogenous danger signals high-mobility group box 1 (HMGB1) and heat shock protein (HSP)70 during wound healing and chronic lymphatic fluid stasis. In a surgical mouse tail model of tissue injury and lymphedema, HMGB1 and HSP70 expression occurred along a spatial gradient relative to the site of injury, with peak expression at the wound and greater than twofold reduced expression within 5 mm (P < 0.05). Expression primarily occurred in cells native to injured tissue. In particular, HMGB1 was highly expressed by lymphatic endothelial cells (>40% positivity; twofold increase in chronic inflammation, P < 0.001). We found similar findings using a peritoneal inflammation model. Interestingly, upregulation of HMGB1 (2.2-fold), HSP70 (1.4-fold), and nuclear factor (NF)-κβ activation persisted at least 6 wk postoperatively only in lymphedematous tissues. Similarly, we found upregulation of endogenous danger signals in soft tissue of the arm after axillary lymphadenectomy in a mouse model and in matched biopsy samples obtained from patients with secondary lymphedema comparing normal to lymphedematous arms (2.4-fold increased HMGB1, 1.9-fold increased HSP70; P < 0.01). Finally, HMGB1 blockade significantly reduced inflammatory lymphangiogenesis within inflamed draining lymph nodes (35% reduction, P < 0.01). In conclusion, HMGB1 and HSP70 are expressed along spatial gradients and upregulated in chronic lymphatic fluid stasis. Furthermore, acute expression of endogenous danger signals may play a role in inflammatory lymphangiogenesis.</AbstractText>
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<ForeName>Victor</ForeName>
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<ForeName>Stephanie</ForeName>
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   |texte=   Temporal and spatial patterns of endogenous danger signal expression after wound healing and in response to lymphedema.
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Temporal and spatial patterns of endogenous danger signal expression after wound healing and in response to lymphedema.

Temporal and spatial patterns of endogenous danger signal expression after wound healing and in response to lymphedema.

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