https://www.journal-of-hepatology.eu/article/S0168-8278(13)00213-4/pdf

Decoding cell death signals in liver inflammation.

Cartilage injury remains a major challenge in orthopedic surgery due to the fact that articular cartilage has only a limited capacity for intrinsic healing. Cartilage impaction is followed by a post-traumatic inflammatory response. Chondrocytes and synoviocytes are activated to produce inflammatory mediators and degradative enzymes which can induce a progradient cartilage self-destruction finally leading to secondary osteoarthritis (OA). However, an anti-inflammatory compensatory response is also detectable in cartilage by up-regulation of anti-inflammatory cytokines, probably a temporary attempt by chondrocytes to restore cartilage homeostasis. Matrix-assisted autologous chondrocyte transplantation (MACT) is a suitable technique for improving the rate of repair of larger articular cartilage defects. For MACT, autologous chondrocytes were isolated from a cartilage biopsy of a non-load bearing joint area. This technique requires sufficient expansion of differentiated autologous chondrocytes, which were then seeded on suitable biodegradable three-dimensional (3D) matrices to preform an extracellular cartilage matrix (ECM) before implantation into the defect. Cell expansion is accompanied by chondrocyte dedifferentiation, whereby substantial changes occur at multiple levels of chondrocyte synthetic profiles: including the ECM, cell surface receptors and cytoskeletal proteins. Since these dedifferentiated chondrocytes produce a non-specific mechanically inferior ECM, they are not suitable for MACT. 3D cultures are means of inducing and maintaining chondrocyte (re)differentiation and to preform ECM. The combination of MACT with anabolic growth factors and anti-inflammatory strategies using anti-inflammatory mediators might be useful for stabilizing the differentiated chondrocyte phenotype, to support neocartilage formation and inhibit post-traumatic cartilage inflammation and hence, the development of secondary OA.

Activation and dedifferentiation of chondrocytes: implications in cartilage injury and repair.

The impact of the local inflammatory response on the process of wound healing has been debated for decades. In particular, the question whether infiltrating macrophages and granulocytes promote or impede tissue repair has received much attention. In the present study, we show that wound healing is accelerated in mice deficient for the anti-inflammatory cytokine interleukin (IL)-10. IL-10−/− mice closed excisional wounds significantly earlier compared with IL-10-competent control littermates. This effect was attributable to accelerated epithelialization as well as enhanced contraction of the wound tissue in the mutant animals. Increased α-smooth muscle actin expression in IL-10-deficient mice suggests that augmented myofibroblast differentiation is responsible for the enhanced contraction of wounds in mutant mice. The number of macrophages infiltrating the wound tissue was significantly increased in IL-10−/− mice compared with control littermates suggesting that this cell type mediates the accelerated tissue repair. These results show for the first time that IL-10 can impede wound repair.

/pdf/accelerated-wound-closure-in-mice-deficient-for-interleukin-3hvdibr8qp.pdf

Accelerated wound closure in mice deficient for interleukin-10.

Methods of treating autoimmune diseases, allergic responses, cancer, or inflammatory diseases in an animal, promoting would healing, repairing epithelial damage and promoting angiogenesis in an organ or tissue of an animal by administering to the animal mesenchymal stem cells in an effective amount.

Mesenchymal stem cells and uses therefor

Tissue regeneration following injury from disease or medical treatment still represents a challenge in regeneration medicine. Prostaglandin E2 (PGE2), which involves diverse physiological processes via E-type prostanoid (EP) receptor family, favors the regeneration of various organ systems following injury for its capabilities such as activation of endogenous stem cells, immune regulation, and angiogenesis. Understanding how PGE2 modulates tissue regeneration and then exploring how to elevate the regenerative efficiency of PGE2 will provide key insights into the tissue repair and regeneration processes by PGE2. In this review, we summarized the application of PGE2 to guide the regeneration of different tissues, including skin, heart, liver, kidney, intestine, bone, skeletal muscle, and hematopoietic stem cell regeneration. Moreover, we introduced PGE2-based therapeutic strategies to accelerate the recovery of impaired tissue or organs, including 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors boosting endogenous PGE2 levels and biomaterial scaffolds to control PGE2 release.

Role of prostaglandin E2 in tissue repair and regeneration.

When we previously examined the participation of local expression of interleukin-10 (IL-10) and tumor necrosis factor-alpha (TNFalpha) in wound healing of an intestinal anastomosis under septic conditions in mice, we found that IL-10 and TNFalpha expressions were markedly enhanced around the anastomosis and that wound healing was impaired in this animal model. The purpose of the present study was to investigate the combined effect of IL-10 on proliferation and remodeling of the extracellular matrix (ECM) of cultured human skin fibroblasts. Human skin fibroblasts were cultured for 48 h with IL-10 and/or TNFalpha at various concentrations, then the proliferation rates were determined using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. The concentration of transforming growth factor-beta1 (TGFbeta1) in cell culture supernatants was measured by enzyme-linked immunosorbent assay, and type I collagen protein and matrix metalloproteinase-I (MMP-I) were detected by indirect immunofluorescence in cultured cells incubated for 48 h with 10 ng/ml of IL-10 and/or 10 ng/ml of TNFalpha. IL-10 itself had no effect on fibroblast proliferation, but reduced TNFalpha-induced fibroblast proliferation. The concentration of TGFbeta1 in cell culture supernatants was significantly lower in the presence of TNFalpha and IL-10 than in the presence of TNFalpha alone. Immunolabeling of fibroblasts for type I collagen protein was decreased in cells incubated with IL-10 and/or TNFalpha compared to controls. MMP-I immunolabeling was increased in cells incubated with IL-10, IL-10 and TNFalpha compared to control and cells incubated with TNFalpha. It is suggested that IL-10 is an inhibitory factor for the remodeling of the ECM during wound healing.

Interleukin-10 Suppresses Proliferation and Remodeling of Extracellular Matrix of Cultured Human Skin Fibroblasts

Ischemia reperfusion (IR) of the liver is a multifactorial process that, at least in part, is responsible for the morbidity associated with major liver surgery under occlusion of the portal triad with the Pringle maneuver, total vascular exclusion or after liver transplantation. Surgeons are confronted with IR injury (IRI) more often than they anticipate. Although the human body has its own defense system, understanding the pathophysiology of IRI is essential for the surgeon in preventing and/or treating the reperfusion injury in common clinical practice. Several endogenous mechanisms exist to overcome IRI and a large number of pharmacological agents have also been found to confer protection against ischemic injury in the liver. They either blocked the injurious pathways directly or they subjected the liver to preconditioning. Prostaglandins (PGs) are a group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase (COX) pathway. They are short-lived, hormone-like chemicals that regulate cellular activities on a moment-to-moment basis and are produced in most tissues of the body, although the liver has emerged as the major organ participating in the synthesis, degradation and elimination of arachidonate products of systemic origin. PGs are released through the prostaglandin transporter on the cell's plasma membrane. During the last decade intensive work on the cytoprotective effects of PGs on livers suffering from IRI have been well documented. Prostaglandins confer their protective effects on IR-injured livers mainly by inhibiting the generation of reactive oxygen species, preventing leukocyte migration, reducing the synthesis or production of membrane degradation products, improving hepatic insulin and lipid metabolism, and regulating the production of inflammatory cytokines and cell adhesion molecules. Production of PGs have been found essential also soon after partial hepatectomy for hepatocyte proliferation.

The role of prostaglandins in liver ischemia-reperfusion injury.

Protective effect of intraportal prostaglandin E1 on prolonged cold preserved rat liver

In previous studies, thermographic findings of breast disease were compared with histological findings for evaluating thermographic usefulness. Some researchers tried to create criteria for thermographic diagnosis of breast disease using many kinds of findings. These trials improved the thermographic accuracy rate, but the criteria became too complex. The first purpose of this study is establishing the standard of thermographic breast cancer detection, which is as simple as possible for commonly used thermography. For this purpose, it is clarified which thermographic findings contributed to breast cancer detection. Then, a diagnostic tree for breast thermography is created. In the second part of this paper, the role of several thermographic findings in breast cancer treatment, is discussed.

https://ieeexplore.ieee.org/iel5/7218/19434/00897950.pdf

Standardization of thermographic breast cancer detection-role of qualitative findings and quantitative findings

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Interleukin-10 Suppresses Proliferation and Remodeling of Extracellular Matrix of Cultured Human Skin Fibroblasts

The role of prostaglandins in liver ischemia-reperfusion injury.

Protective effect of intraportal prostaglandin E1 on prolonged cold preserved rat liver

Standardization of thermographic breast cancer detection-role of qualitative findings and quantitative findings