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At least 667 records · Page 37Linked to original sources
PubMed2005

Lysyl oxidase in development, aging and pathologies of the skin.

Lysyl oxidase (LOX) is a copper- and lysyl-tyrosyl cofactor containing amine oxidase that has been known to play a critical role in the catalysis of lysine-derived crosslinks in extracellular matrix (ECM) proteins in the dermis. Changes in the composition and crosslinked state of the ECM and alterations in LOX synthesis and activity are known to be associated with aging and a range of acquired and heritable skin disorders. It has been assumed until recently that the LOX-related changes in the skin are mediated through the catalytic activity of LOX. However, work by several laboratories over the last few years has shown that LOX is a multifunctional protein. In this review we discuss the regulation of expression, localization and activation of LOX in the normal developing and adult skin, and alterations in LOX expression and activity associated with skin aging and senescence, and in pathological conditions, including wound healing, fibrosis, hypertrophic scarring, keloids, scleroderma, and diabetic skin. We further evaluate the role of LOX in skin ECM changes associated with the normal aging process and with these pathological states. In addition to collagen and elastin cross-linkages, regulatory and activation mechanisms and cell type specific LOX interactions may contribute to a range of novel intra- and extracellular LOX functions that appear critical determinants of the cellular microenvironment in the normal skin and in these skin disorders.

Adult↗
PubMed1998

Aneuploidy analysis in fibroblasts of human premature aging syndromes by FISH during in vitro cellular aging.

Cultured cells from human premature aging syndromes show premature replicative senescence and as such might serve as models for genetic studies of cellular replicative senescence/aging. To date, no systematic study on chromosome-specific aneuploidy in premature aging syndromes has been carried out using molecular-cytogenetic techniques. We, therefore, have performed a comparative analysis of chromosome-specific aneuploidy levels at both interphase and metaphase in earlier (younger) and later (older) passage fibroblasts from two normal male and female versus six male and female premature aging syndromes (Cockayne, Hutchinson-Gilford and Werner) by FISH. We have used seven chromosome-specific DNA probes (nos. 1, 4, 6, 8, 10, 15, X) and four DNA probes (nos. 1, 4, 6, X) for females and males, respectively. Our data on total aneuploidy of each chromosome in all cell cultures indicated that significantly higher percentages of aneuploid cells were detectable at interphase than at metaphase. Also, the interphase aneuploidy levels of all chromosomes under study were significantly higher in cells from the syndromes as compared to these of the normal controls at both earlier and later passages. In general, the interphase aneuploidy level of each of the chromosomes in both the control and experimental cell cultures increased with in vitro proliferation and aging, although to a much lesser extent in the controls. The aneuploidy levels, however, varied widely from chromosome to chromosome in each case. Since adequate numbers of mitotic cells were not always available in some later passage cells of various premature aging syndromes, metaphase chromosome analysis for all chromosomes under study was not always possible at this stage, but interphase cytogenetics was very informative in all cases. No consistent pattern of chromosome-specific aneuploidy was detected in the earlier passage cells (younger cells) of the syndromes. However, the later passage cells (older cells) from all three female syndromes consistently showed the highest aneuploidy levels for the X chromosome at interphase.

Adolescent↗
PubMed1988

Decline of fibroblast chemotaxis with age of donor and cell passage number.

Human dermal fibroblasts have a limited life span in culture, which is manifested by a progressive decline of their proliferative activity. Here we show by the Boyden Chamber assay that the chemotactic response of human fibroblasts to fibroblast-conditioned medium and fibronectin declines during cellular aging in vitro and in vivo. The chemotactic response of human embryonic fibroblasts (HEF) declined progressively after the 25th passage. Virtually no chemotactic activity could be observed after the 40th passage in culture. Fibroblasts cultures from donors aged between 70-90 years had lost chemotactic activity by the 15th passage. Cells from patients suffering from progeroid syndromes of premature aging showed, even in early passages, a very low chemotactic response (20% of the HEF) and lost their chemotactic activity after a few subcultures. The response to the chemoattractant fibronectin also decreased with aging. Immunofluorescence studies indicated that the decline in chemotactic activity was accompanied by the formation of a thicker fibronectin network in the extracellular matrix of senescent human fibroblasts and progeroid cells than that observed in early passage embryonic cultures. Since fibroblast chemotaxis and synthesis of connective tissue components probably play an important role in tissue repair, our results could contribute to an understanding of age-related differences in the healing of skin wounds.

Aged↗
PubMed2000

The accelerated occurrence of age-related changes of organism in Chernobyl workers: a radiation-induced progeroid syndrome?

The rate of aging was studied in 306 persons working at Chernobyl Atomic Power Station after the accident by means of integral and partial biological age assessment. An accelerated rate of aging was found in 81% of men and in 77% of women in comparison with a control random population sample of Kiev. Persons younger than 45 years appeared to be more vulnerable to radiation. The biological age of persons who worked in the contaminated zone immediately after the disaster exceeded the biological age in those who arrived in Chernobyl 4 months later. The biological age in the investigated persons exceeded its average populational value for 5 years (the integral biological and partial cardiopulmonary age) and for 11 years for the partial psychological age. These data may underlie the concept of radiation progeroid syndrome as the form of accelerated aging.

Abnormalities, Radiation-Induced↗
PubMed1998

A DNA repair defect in a patient with ataxia, mental retardation, and short stature.

A 12-year-old girl developed ataxia that gradually progressed. At age 18 the patient presented with mental retardation, cachectic dwarfism, microcephalus, and a progeroid appearance but no photosensitive skin lesions or deafness. On analysis of fibroblasts, unscheduled DNA synthesis was reduced to 50% of normal, but colony-forming ability after ultraviolet irradiation was normal. The symptoms and phenotype of the patient were distinguished from those in Cockayne syndrome and xeroderma pigmentosum. This case is interesting because the defect in DNA repair after ultraviolet irradiation was detected in a patient with neurologic disturbances but without photosensitive skin lesions.

Abnormalities, Multiple↗