Understanding the molecular and cellular processes in skin wound healing can pave the way for devising innovative concepts by turning the identified natural effectors into therapeutic tools. Based on the concept of broad‑scale engagement of members of the family of galactoside‑binding lectins (galectins) in pathophysiological processes, such as cancer or tissue repair/regeneration, the present study investigated the potential of galectins‑1 (Gal‑1) and ‑3 (Gal‑3) in wound healing. Human dermal fibroblasts, which are key cells involved in skin wound healing, responded to galectin exposure (Gal‑1 at 300 or Gal‑3 at 600 ng/ml) with selective changes in gene expression among a panel of 84 wound‑healing‑related genes, as well as remodeling of the extracellular matrix. In the case of Gal‑3, positive expression of Ki67 and cell number increased when using a decellularized matrix produced by Gal‑3‑treated fibroblasts as substrate for culture of interfollicular keratinocytes. In vivo wounds were topically treated with 20 ng/ml Gal‑1 or ‑3, and collagen score was found to be elevated in excisional wound repair in rats treated with Gal‑3. The tensile strength measured in incisions was significantly increased from 79.5±17.5 g/mm2 in controls to 103.1±21.4 g/mm2 after 21 days of healing. These data warrant further testing mixtures of galectins and other types of compounds, for example a combination of galectins and TGF‑β1.

• Klíčová slova
• extracellular matrix, fibroblast, keratinocyte, lectin, regeneration,
• MeSH
• fibroblasty metabolismus   patologie   MeSH
• galektiny biosyntéza   MeSH
• kolagen biosyntéza   MeSH
• krevní proteiny biosyntéza   MeSH
• lidé MeSH
• pevnost v tahu * MeSH
• rány a poranění metabolismus   patologie   MeSH
• regulace genové exprese * MeSH
• škára metabolismus   patologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• galektiny MeSH
• kolagen MeSH
• krevní proteiny MeSH
• LGALS3 protein, human MeSH Prohlížeč

Similarly to other types of malignant tumours, the incidence of head and neck cancer is increasing globally. It is frequently associated with smoking and alcohol abuse, and in a broader sense also with prolonged exposure to these factors during ageing. A higher incidence of tumours observed in younger populations without a history of alcohol and tobacco abuse may be due to HPV infection. Malignant tumours form an intricate ecosystem of cancer cells, fibroblasts, blood/lymphatic capillaries and infiltrating immune cells. This dynamic system, the tumour microenvironment, has a significant impact on the biological properties of cancer cells. The microenvironment participates in the control of local aggressiveness of cancer cells, their growth, and their consequent migration to lymph nodes and distant organs during metastatic spread. In cancers originating from squamous epithelium, a similarity was demonstrated between the cancer microenvironment and healing wounds. In this review, we focus on the specificity of the microenvironment of head and neck cancer with emphasis on the mechanism of intercellular crosstalk manipulation for potential therapeutic application.

• Klíčová slova
• IL-6, cancer, cancer ecosystem, cancer microenvironment, cancer therapy, cancer-associated fibroblast, cytokine, extracellular matrix, tumour-associated macrophages,
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Estrogen deprivation is considered responsible for many age-related processes, including poor wound healing. Guided by previous observations that estradiol accelerates re‑epithelialization through estrogen receptor (ER)‑β, in the present study, we examined whether selective ER agonists [4,4',4''-(4-propyl [1H] pyrazole-1,3,5-triyl)‑trisphenol (PPT), ER‑α agonist; 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), ER‑β agonist] affect the expression of basic proliferation and differentiation markers (Ki‑67, keratin‑10, ‑14 and ‑19, galectin‑1 and Sox‑2) of keratinocytes using HaCaT cells. In parallel, ovariectomized rats were treated daily with an ER modulator, and wound tissue was removed 21 days after wounding and routinely processed for basic histological analysis. Our results revealed that the HaCaT keratinocytes expressed both ER‑α and ‑β, and thus are well-suited for studying the effects of ER agonists on epidermal regeneration. The activation of ER‑α produced a protein expression pattern similar to that observed in the control culture, with a moderate expression of Ki‑67 being observed. However, the activation of ER‑β led to an increase in cell proliferation and keratin‑19 expression, as well as a decrease in galectin‑1 expression. Fittingly, in rat wounds treated with the ER‑β agonist (DPN), epidermal regeneration was accelerated. In the present study, we provide information on the mechanisms through which estrogens affect the expression patterns of selected markers, thus modulating keratinocyte proliferation and differentiation; in addition, we demonstrate that the pharmacological activation of ER-α and -β has a direct impact on wound healing.

• MeSH
• alfa receptor estrogenů agonisté   metabolismus   MeSH
• beta receptor estrogenů agonisté   metabolismus   MeSH
• buněčná diferenciace účinky léků   MeSH
• buněčné linie MeSH
• fenoly farmakologie   MeSH
• hojení ran účinky léků   MeSH
• keratinocyty cytologie   účinky léků   metabolismus   patologie   MeSH
• kůže účinky léků   metabolismus   patologie   MeSH
• lidé MeSH
• nitrily farmakologie   MeSH
• potkani Sprague-Dawley MeSH
• pyrazoly farmakologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 2,3-bis(4-hydroxyphenyl)-propionitrile MeSH Prohlížeč
• 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol MeSH Prohlížeč
• alfa receptor estrogenů MeSH
• beta receptor estrogenů MeSH
• fenoly MeSH
• nitrily MeSH
• pyrazoly MeSH