Calcium: a potential central regulator in wound healing in the skin

  title={Calcium: a potential central regulator in wound healing in the skin},
  author={Alan B. G. Lansdown},
  journal={Wound Repair and Regeneration},
  • A. Lansdown
  • Published 1 September 2002
  • Biology, Medicine
  • Wound Repair and Regeneration
Calcium has an established role in the normal homeostasis of mammalian skin and serves as a modulator in keratinocyte proliferation and differentiation. Gradients of calcium concentration increasing from 0.5 mM in the basal layer to > 1.4 mM in the stratum granulosum are consistent with migration patterns in response to minor abrasion (normal wear). Dermal fibroblasts require calcium but are approximately 100 times less sensitive than keratinocytes. Normal calcium metabolism in the skin is… 
The Role of Calcium in Wound Healing
This review explores the functions and roles of calcium in skin regeneration and reconstruction during would healing and investigates the possibility of incorporating calcium into scaffolds and examines how it modulates cutaneous wound healing.
Zinc in wound healing: Theoretical, experimental, and clinical aspects
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Wound Healing: A Cellular Perspective.
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Calmodulin-like protein upregulates myosin-10 in human keratinocytes and is regulated during epidermal wound healing in vivo.
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Calreticulin enhances porcine wound repair by diverse biological effects.
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Ex vivo calcium percutaneous eggression in normal and tape-stripped human skin
This ex vivo method reproduced the increased of calcium skin permeability with a disrupted barrier and developed a non-invasive method to measure calcium flux concentration in normal and damaged skin that might be reproduced and validated in vivo.
Targeted inhibition of endothelial calpain delays wound healing by reducing inflammation and angiogenesis
It is shown that endothelial calpain-1/2 disruption is associated with reduced injury-activated inflammation, reduced CD31+ blood vessel density, and delayed wound healing, and delineate a novel mechanistic role for calpain in the crosstalk between inflammation and angiogenesis during skin repair.
Mesoglycan induces keratinocyte activation by triggering syndecan‐4 pathway and the formation of the annexin A1/S100A11 complex
It is found that mesoglycan induces keratinocyte migration and early differentiation by triggering the syndecan‐4/PKCα pathway and that these effects were at least in part, because of the formation of the annexin A1/S100A11 complex.
Autologous platelets as a source of proteins for healing and tissue regeneration.
The aim is to discuss the ways in which platelets may provide such unexpected beneficial therapeutic effects in clinical situations requiring rapid healing and tissue regeneration.


Increased calcium levels alter cellular and molecular events in wound healing.
These studies define the molecular and cellular events occurring as a result of the addition of elevated levels of calcium both in vitro and in vivo, which may play a key role in the pathogenesis of chronic wounds.
Sequential changes in trace metal, metallothionein and calmodulin concentrations in healing skin wounds
Increases in metallothionein immunoreactivity are demonstrated as an indication of zinc and copper activity in the papillary dermis and in basal epidermal cells near the wound margin 1–5 d after wounding, consistent with metalloenzyme requirements in inflammation and fibrogenesis.
Psoriasis and altered calcium metabolism: downregulated capacitative calcium influx and defective calcium-mediated cell signaling in cultured psoriatic keratinocytes.
Psoriatic keratinocytes have an inborn error in calcium metabolism, rather than a localized defect in response to altered extracellular calcium gradient observed in vivo, suggesting defective capacitative calcium influx of psoriatic cells.
Increased calmodulin levels in psoriasis and low Ca++ regulated mouse epidermal keratinocyte cultures.
Increased calmodulin levels are suggested to be associated with epidermal hyperproliferation and/or with the state of differentiation in psoriasis.
Differences in the regulation of intracellular calcium in normal and neoplastic keratinocytes are not caused by ras gene mutations.
To determine whether the activating c-rasHa mutation in 308 and SP-1 cells was responsible for the altered Cai regulation, a v-ras Ha gene was introduced into normal keratinocytes by a defective retrovirus and it was found that these cells were resistant to Ca(2+)-induced terminal differentiation.
Calcium and potassium are important regulators of barrier homeostasis in murine epidermis.
It is demonstrated that the repair of the epidermal permeability barrier after solvent disruption can be prevented by calcium, potassium, and phosphate.
Shifts in the concentrations of magnesium and calcium in early porcine and rat wound fluids activate the cell migratory response.
Wound fluids collected throughout the early stages of cutaneous wound repair were examined for possible Mg2+ and Ca2+ fluctuations to suggest that the impact of these changes on integrins and E-cadherin may play a direct role in the activation and maintenance of the migratory phenotypes of the cells involved in the wound healing process.
Normalization of epidermal calcium distribution profile in reconstructed human epidermis is related to improvement of terminal differentiation and stratum corneum barrier formation.
It is demonstrated that improvement of the stratum corneum barrier properties in vitro is concurrent with the normalization of the epidermal calcium gradient, whereas deregulation of terminal differentiation correlates with an accumulation of calcium ions within incompletely differentiated corneocytes.