Stem Cell Treatments ‘Go Deep’ to Regenerate Sun-Damaged Skin

AHA Publisher — Mon, 01 Jun 2020 07:00:12 +0000

Wolters Kluwer Health via EurekAlert – For a while now, some plastic surgeons have been using stem cells to treat aging, sun-damaged skin. But while they’ve been getting good results, it’s been unclear exactly how these treatments – using adult stem cells harvested from the patient’s own body – work to rejuvenate “photoaged” facial skin. A new microscopic-level study provides the answer: within a few weeks, stem cell treatment eliminates the sun-damaged elastin network and replacing them with normal, undamaged tissues and structures – even in the deeper layers of skin. Injection of the patient’s own mesenchymal stem cells (MSCs) is “appropriate, competent and sufficient to elicit the full structural regeneration of the sun-aged skin,” according to the report by Dr. Luis Charles-de-Sá, MD, of Universidade Federal do Rio de Janeiro, Brazil, Natale Gontijo-Amorim, MD and Gino Rigotti, MD of Verone-Italy University and colleagues. Their study appears in the June issue of Plastic and Reconstructive Surgery®, the official medical journal of the American Society of Plastic Surgeons (ASPS). The researchers assessed the cellular- and molecular-level effects of MSC treatment on sun-damaged (photoaged) facial skin. All 20 patients in the study, average age 56 years, were scheduled for facelift surgery. The patients lived in northeast Brazil, a region where intense sun exposure is expected. For each patient, a small sample of fat cells from the abdomen was processed to create patient-specific MSCs. The cultured stem cells were injected under the skin of the face, in front of the ear. When the patients underwent facelift surgery three to four months later, skin samples from the stem cell-treated area were compared to untreated areas. Histologic and structural under the microscope analysis demonstrated that MSC treatment led to improvement in overall skin structure. Treated areas showed “partial or extensive reversal” of sun-related damage to the skin’s stretchy elastin network – the main skin structure affected by photoaging. In the layer immediately beneath the skin surface, the stem cell-treated areas showed regeneration of a new, fully organized network of fiber bundles and dermal ECM remodeling changes. In the deeper skin layer, “tangled, degraded, and dysfunctional” deposits of sun-damaged elastin were replaced by a normal elastin fiber network. These changes were accompanied by molecular markers of processes involved in absorbing the abnormal elastin and development of new elastin. The findings suggested that stem cells triggered each of the many cellular- and molecular-level pathways involved in skin repair and regeneration. Use of the patient’s own fat-derived MSCs “may be a relevant proposal for the anti-ageing action in regeneration of photodamaged human skin,” Dr. Charles-de-Sá and colleagues write. “The researchers conclude that stem-cells can lead to regeneration of sun-aged skin,” according to a video commentary by Plastic and Reconstructive Surgery Editor-in-Chief Rod J. Rohrich, MD. In his video, Dr. Rohrich walks viewers through the dramatic changes in the microscopic appearance of skin samples obtained before and after MSC treatment. “The re-building of structures below the surface translates to true improvements to the strength and appearance of the facial dermis,” Dr. Rohrich adds. He emphasizes that patients interested in stem-cell treatment for aging, sun-damaged skin should discuss their options with a Board-certified plastic surgeon. To read the original article click here.

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U of L Researchers Describe Possible Mechanism for Link Between Obesity and Breast Cancer

AHA Publisher — Mon, 13 Apr 2020 07:00:35 +0000

University of Louisville via EurekAlert – Researchers publish theory that specific protein from adipose tissue promotes breast cancer development. LOUISVILLE, Ky. – It is widely accepted that higher levels of body fat increase the risk of developing breast cancer, as well as other cancers. Based on his ongoing research, Bing Li, Ph.D., has published an article which proposes a unique theory that a protein secreted by fat cells drives the development of breast cancer. Li has been conducting research funded by the National Cancer Institute for the past five years which led him to the connection between activity of a protein expressed in fatty tissue and an increase in breast cancer development. Li and colleagues shared the theory in an invited forum in Trends in Molecular Medicine, a Cell Press journal, published online last week. The article describes Li’s theory that adipose fatty acid binding protein (FABP4), expressed in fatty tissue, is responsible for fueling breast cancer tumor growth. “Many types of cancer are related to obesity, not only breast cancer. More than 13 types of cancer are clearly associated with obesity and I think the list will go on and on once we have more data,” Li said. “In our research, we found the fatty acid binding protein family, especially one member, FABP4, plays a very critical role in the association of obesity and cancer, most specifically breast cancer. We theorize that FABP4 is responsible for the underlying molecular mechanism which promotes obesity-associated breast cancer development.” Adipose tissue in the body produces FABP4 within fat cells, where it processes and distributes water-insoluble long-chain fatty acids. A certain amount of FABP4 enters the bloodstream under normal conditions. However, as a higher volume of fat tissue is accumulated, more FABP4 is secreted into circulation. “When we get obese, this protein is secreted out much more into the circulatory system,” Li said. “Normally these molecules are inside the cells, but when people are obese, the molecules are outside.” Li’s theory offers two ways in which FABP4 may stimulate growth in breast cancer tumors. First, within the cells, FABP4 increases in certain tumor-associated macrophages, which accumulate in tumors to promote tumor growth. Li’s research also revealed that when FABP4 is inhibited, tumor growth is reduced in animal models even though the adipose tissue remained. Second, when elevated levels of FABP4 circulate outside the fat cells in obesity, the protein promotes breast cancer development through direct interaction with breast cancer cells. In animal research, mammary tumor development and growth were reduced in obese animals in which FABP4 was controlled. In addition, FABP4 in the bloodstream appears to work in multiple mechanisms to fuel interactions between tumor components and fat cells, thereby promoting cancer development. Moreover, Li’s research group recently published findings in Cancer Research showing that different types of high-fat diets have different effects on tumor development. High-fat diets of either cocoa butter or fish oil both result in fat-induced obesity. However, the cocoa butter diet results in increased mammary tumor growth, while the fish oil diet does not. This study not only confirms the critical role of FABP4 in obesity-associated cancer, but reveals that not all obesity promotes the development of tumors. Li and his team believe a better understanding of how FABP4 works both within macrophages and in circulation could provide opportunities to prevent certain breast cancers from progressing. It may also lead to the development of treatment methods that target FABP4 with drugs or specific antibodies. “Now we are trying to generate some antibodies for this protein, which could be a very effective therapy strategy for obesity-associated cancer,” Li said. To read the original article click here.

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Stem Cell Treatments ‘Go Deep’ to Regenerate Sun-Damaged Skin

U of L Researchers Describe Possible Mechanism for Link Between Obesity and Breast Cancer