Beta‐adrenoceptor blockade delays granulation tissue formation in polyurethane sponge implants

Romana‐Souza, Bruna; Santos, Jeanine Salles dos; Desmoulière, Alexis; Monte‐Alto‐Costa, Andréa

doi:10.1111/j.1600-0560.2008.01110.x

Cited by 3 publications

(13 citation statements)

References 23 publications

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“…One of the first events of granulation tissue formation is angiogenesis, where endothelial cells proliferate and develop a blood vessel network that sustains the development of granulation tissue. The control + propranolol group presented an increased number of blood vessels 14 days after wounding, similar to previous studies where propranolol administration delays angiogenesis in non‐stressed rats (17,18,32). Stress group presented an elevated number of blood vessels over the course of the experiment, whereas stress + propranolol group presented blood vessels number similar to control group.…”

Section: Discussionsupporting

confidence: 89%

“…interleukin‐1β (IL‐1β) and TNF‐α), which stimulate granulation tissue formation (35). The control + propranolol group presented a delay in the inflammatory cell migration and an increase in the TNF‐α expression confirming data in the literature (17,18,32). In the stress group, inflammatory cell number and TNF‐α expression were reduced 7 days after wounding, but were increased 14 days after wounding.…”

Section: Discussionsupporting

confidence: 88%

“…Some of those cells differentiate in myofibroblasts, which perform wound contraction (54). The control + propranolol group presented delayed connective tissue cell proliferation, increased myofibroblast differentiation and reduced collagen deposition, as observed in previous studies (17,18,32). Stress group presented an elevated number of proliferating connective tissue cells and myofibroblasts until 14 days after wounding, but a less organized and dense collagen scaffold.…”

Section: Discussionsupporting

confidence: 85%

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Cutaneous wound healing of chronically stressed mice is improved through catecholamines blockade

Romana‐Souza

Pôrto

Monte‐Alto‐Costa

2010

Experimental Dermatology

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Stress impairs cutaneous wound healing; however, it is unclear how beta-adrenoceptors participates in alterations induced by stress on skin wound repair. Therefore, the aim of this study was to investigate the effects of propranolol, a non-selective beta-blocker, administration on cutaneous wound healing of chronically stressed mice. Male mice were spun at 115 rpm for 15 min every hour from three days before wounding until euthanasia. Control animals were not submitted to stress. Stressed and control animals were treated with propranolol dissolved in water; controls received only water. Propranolol administration began one day before wounding and was continued daily until euthanasia. A full-thickness excisional lesion was performed. Seven and fourteen days later, animals were killed, and lesions were formalin-fixed and paraffin-embedded. Sections were stained with hematoxylin-eosin and immunostained against F4/80 to quantify macrophages, alpha-smooth muscle actin to quantify the myofibroblast density and proliferating cell nuclear antigen to quantify the cell proliferation. Furthermore, matrix metalloproteinases (MMP)-2 and MMP-9 activity, nitrite and hydroxyproline levels and tumor necrosis factor-alpha (TNF-alpha) expression were measured in wound. Stress and control + propranolol groups presented a delay in wound contraction, re-epithelialization, F4/80-positive macrophages, neutrophils and mast cells infiltration, cellular proliferation, angiogenesis, myofibroblastic differentiation, MMP-2 and MMP-9 activation and TNF-alpha expression, whereas an increase in the nitrite levels. Stress + propranolol group presented results similar to control group. In conclusion, stress impairs cutaneous wound healing in mice through beta1- adrenoceptors and beta2-adrenoceptors activation.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 85%

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Cutaneous wound healing of chronically stressed mice is improved through catecholamines blockade

Romana‐Souza

Pôrto

Monte‐Alto‐Costa

2010

Experimental Dermatology

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“…Several studies have demonstrated that β‐adrenoceptors strongly participate in cutaneous wound healing (Pullar & Isseroff ; Romana‐Souza et al . ,b; Pullar et al . ).…”

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confidence: 99%

“…Other studies have shown that β1/β2‐adrenoceptor blockade delays wound contraction and re‐epithelialization in rats, and granulation tissue development in polyurethane (PU) sponge implants (Romana‐Souza et al . b,c). Nevertheless, β2‐adrenoceptor deletion may promote wound angiogenesis and re‐epithelialization in mice (Pullar et al .…”

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confidence: 99%

Deletion of the α2A/α2C‐adrenoceptors accelerates cutaneous wound healing in mice

Romana‐Souza

Nascimento

Brum

et al. 2014

Int J Experimental Path

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The α2-adrenoceptors regulate the sympathetic nervous system, controlling presynaptic catecholamine release. However, the role of the α2-adrenoceptors in cutaneous wound healing is poorly understood. Mice lacking both the α2A/α2C-adrenoceptors were used to evaluate the participation of the α2-adrenoceptor during cutaneous wound healing. A full-thickness excisional lesion was performed on the dorsal skin of the α2A/α2C-adrenoceptor knockout and wild-type mice. Seven or fourteen days later, the animals were euthanized and the lesions were formalin-fixed and paraffin-embedded or frozen. Murine skin fibroblasts were also isolated from α2A/α2C-adrenoceptor knockout and wild-type mice, and fibroblast activity was evaluated. The in vivo study demonstrated that α2A/α2C-adrenoceptor depletion accelerated wound contraction and re-epithelialization. A reduction in the number of neutrophils and macrophages was observed in the α2A/α2C-adrenoceptor knockout mice compared with wild-type mice. In addition, α2A/α2C-adrenoceptor depletion enhanced the levels of nitrite and hydroxyproline, and the protein expression of transforming growth factor-β and vascular endothelial growth factor. Furthermore, α2A/α2C-adrenoceptor depletion accelerated blood vessel formation and myofibroblast differentiation. The in vitro study demonstrated that skin fibroblasts isolated from α2A/α2C-adrenoceptor knockout mice exhibited enhanced cell migration, α-smooth muscle actin _protein expression and collagen deposition compared with wild-type skin fibroblasts. In conclusion, α2A/α2C-adrenoceptor deletion accelerates cutaneous wound healing in mice.

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Propranolol impairs the closure of pressure ulcers in mice

2014

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Beta‐adrenoceptor blockade delays granulation tissue formation in polyurethane sponge implants

Abstract: Blockade of beta1- and beta2-adrenoceptors, but not alpha-adrenoceptors, impairs granulation tissue development in PU implants due to interference with the inflammatory response.

Cited by 3 publications

References 23 publications

Cutaneous wound healing of chronically stressed mice is improved through catecholamines blockade

Cutaneous wound healing of chronically stressed mice is improved through catecholamines blockade

Deletion of the α2A/α2C‐adrenoceptors accelerates cutaneous wound healing in mice

Propranolol impairs the closure of pressure ulcers in mice

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