Skin microvascular adaptations during maturation and aging of hairless mice

Vollmar, Brigitte; Morgenthaler, Martin; Amon, M.; Menger, Michael D.

doi:10.1152/ajpheart.2000.279.4.h1591

Cited by 22 publications

(29 citation statements)

References 15 publications

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“…In a previous investigation [18], we demonstrated that 75 % of immunocompetent homozygous hairless mice (skh-1) died a natural death within a 72-week period. Accordingly, 19-month-old (76-week-old) animals were considered to be senescent.…”

Section: Animalsmentioning

confidence: 89%

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Aging is associated with an increased susceptibility to ischaemic necrosis due to microvascular perfusion failure but not a reduction in ischaemic tolerance

et al. 2007

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In the present study in a murine model of chronic ischaemia, we analysed: (i) whether aging was associated with an increased susceptibility to ischaemic necrosis, and (ii) whether this was based on microvascular dysfunction or reduced ischaemic tolerance. An ischaemic pedicled skin flap was created in the ear of homozygous hairless mice. The animals were assigned to three age groups, including adolescent (2±1 months), adult (10±2 months) and senescent (19±3 months). Microvascular perfusion of the ischaemic flap was assessed over 5 days by intravital microscopy, evaluating FCD (functional capillary density), capillary dilation response and the area of tissue necrosis. Expression of the stress-protein HO (haem oxygenase)-1 was determined by immunohistochemistry and Western blotting. Induction of chronic ischaemia stimulated a significant expression of HO-1 without a significant difference between the three age groups. This was associated with capillary dilation, which, however, was more pronounced in adolescent (10.5±2.8 μm compared with 3.95±0.79 μm at baseline) and adult (12.1±3.1 μm compared with 3.36±0.45 μm at baseline) animals compared with senescent animals (8.5±1.7 μm compared with 3.28±0.69 μm at baseline; P value not significant). In senescent animals, flap creation further resulted in complete cessation of capillary flow in the distal area of the flap (FCD, 0±0 cm/cm2), whereas adult (11.9±13.5 cm/cm2) and, in particular, adolescent animals (58.4±33.6 cm/cm2; P<0.05) were capable of maintaining residual capillary perfusion. The age-associated microcirculatory dysfunction resulted in a significantly increased flap necrosis of 49±8% (P<0.05) and 42±8% (P<0.05) in senescent and adult animals respectively, compared with 31±6% in adolescent mice. Of interest, functional inhibition of HO-1 by SnPP-IX (tin protoporphyrin-IX) in adolescent mice abrogated capillary dilation, decreased functional capillary density and aggravated tissue necrosis comparably with that observed in senescent mice. Thus aging is associated with an increased susceptibility to tissue necrosis, which is due to a loss of vascular reactivity to endogenous HO-1 expression, rather than a reduction in ischaemic tolerance.

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Section: Animalsmentioning

confidence: 89%

“…Accordingly, 19-month-old (76-week-old) animals were considered to be senescent. In analogy with other previous studies [18], 2-month-and 10-month-old animals were considered adolescent and adult respectively.…”

Section: Animalsmentioning

confidence: 99%

Aging is associated with an increased susceptibility to ischaemic necrosis due to microvascular perfusion failure but not a reduction in ischaemic tolerance

et al. 2007

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show abstract

Section: Animalsmentioning

confidence: 99%

“…We, therefore, accounted for two distinct conditions associated with skh-1-mice: (1) 75% of immunocompetent homozygous hairless mice (skh-1) died of a natural death within a 72-week period [15]. Accordingly, 19-month-old animals (76 weeks old) have to be regarded as senescent, whereas 2-and 10-month-old animals were considered adolescent and adult, respectively [15]. (2) Furthermore, we rely on the fact that the absolute number and the general pattern of vessels within the defined tissue areas is fixed within the late juvenile growth phase [15].…”

Section: Animalsmentioning

confidence: 99%

“…Accordingly, 19-month-old animals (76 weeks old) have to be regarded as senescent, whereas 2-and 10-month-old animals were considered adolescent and adult, respectively [15]. (2) Furthermore, we rely on the fact that the absolute number and the general pattern of vessels within the defined tissue areas is fixed within the late juvenile growth phase [15].…”

Section: Animalsmentioning

confidence: 99%

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Gender-specific ischemic tissue tolerance in critically perfused skin

Harder

Amon

Wettstein

et al. 2009

Langenbecks Arch Surg

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Purpose The purpose of this study is to determine genderspecific differences in the development of necrosis in persistent ischemic tissue and to analyze whether differences are due to gender-specific loss of vascular reactivity or change in ischemic tolerance. Methods Hairless mice (skh-1) of both genders were assigned to three groups of adolescent, adult, and senescent age. Critical ischemia was induced by transection of the two distal pedicles of the animal's ear. Microcirculation was assessed over a 5-day period using intravital epifluorescence microscopy. Tissue necrosis, blood flow, functional capillary density (FCD), red blood cell (RBC) velocity, and capillary diameter were analyzed. Results Induction of persistent ischemia caused an agedependent demarcation of nonperfused flap tissue. Adult and senescent females developed markedly more necrosis than age-matched males (49±1% vs. 37±3% and 53±3% vs. 44±2%, respectively; p<0.05), whereas no genderspecific difference in flap necrosis was observed in adolescent animals (31±2% vs. 33±3%). Gender did not affect the amount of microcirculatory dysfunction in the flap. Thus, age-matched females and males exhibited a comparable decrease of FCD, RBC velocity, and capillary dilatory response. Conclusions Both age and female gender may predispose for an increased susceptibility to develop ischemic tissue necrosis. The increased necrosis in female animals does not apply to an aggravated microvascular dysfunction, but rather to a reduced ischemic tissue tolerance.

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Effects of a sunscreen formulation on albino hairless mice: a morphological approach

et al. 2013

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The purpose of the study was to evaluate the effects of a sunscreen formulation on the skin of albino hairless mice subjected to simulated solar light (SSL) in terms of morphological changes. Young adult albino hairless mice HRS/J (n = 36) were used as an experimental model for determining skin photoaging changes. Mice were irradiated with SSL, and the sunscreen (estimated SPF 30, PF-UVA) was obtained from the Pharmacy College/UFRJ, Brazil. The animals were divided into four groups: non-treated (G1), radiation only (G2), sunscreen-treated (G3) and vehicle + radiation (G4). Animals from groups G2, G3 and G4 were irradiated weekly (5 weeks), with no immobilization. One week after the final exposure, the dorsal skin was observed using a dermatoscopic camera. Biopsies were analyzed in order to quantify neovascularization and to evaluate histological aspects of the skin. Neovascularization was also evaluated with immunohistochemical reactions for the Von Willebrand factor. Animals from G2 displayed classical morphological changes denoting skin photoaging: thickening of the epidermis, increased dermal cellularity, follicular keratosis, sebaceous gland hyperplasia, and angiogenesis. Animals from groups G3 and G1 displayed similar morphological profiles, without these changes. Animals from group G4 showed more morphological changes than group G2, emphasizing the relative importance of the putative photosensitizing components present in the vehicle formulation. The extent of the morphological skin changes suggested that the sunscreen formulation was effective against SSL, and showed the importance of assessing the phototoxicity of vehicle formulations.

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Skin microvascular adaptations during maturation and aging of hairless mice

Cited by 22 publications

References 15 publications

Aging is associated with an increased susceptibility to ischaemic necrosis due to microvascular perfusion failure but not a reduction in ischaemic tolerance

Aging is associated with an increased susceptibility to ischaemic necrosis due to microvascular perfusion failure but not a reduction in ischaemic tolerance

Gender-specific ischemic tissue tolerance in critically perfused skin

Effects of a sunscreen formulation on albino hairless mice: a morphological approach

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