Splenic lipofuscinosis in mice

Crichton, David; Busuttil, A.; Price, W. H.

doi:10.1002/path.1711260210

Cited by 16 publications

(10 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To assess aortic fatty streak lesion development, all sections were stained with oil red O and quantitatively examined for lipid deposition in the wall of the aortic root as previously described (15)(16)(17) ( 19). The absence ofthis property may be related to the degree of oxidation or polymerization of lipofuscin components.…”

Section: Methodsmentioning

confidence: 99%

“…Quantitative assessment of aortic fatty streak formation in the (BXH) RI strains revealed nonparental phenotypes (Table VII), indicating the involvement of multiple independent genetic factors or a major genetic effect with modi- (19,27). In contrast to cardiac lipofuscin, the occurrence of splenic lipofuscin in C57BL/6J and related strains was only 10-50%, making genetic analysis difficult.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Involvement of the tyrosinase gene in the deposition of cardiac lipofuscin in mice. Association with aortic fatty streak development.

Qiao

Welch²,

Xie³

et al. 1993

J. Clin. Invest.

View full text Add to dashboard Cite

Lipofuscin pigment, a terminal oxidation product, accumulates within cells during the normal aging process and under certain pathological conditions. We have analyzed a genetic cross between two inbred mouse strains, BALB/cJ and a subline of C57BL/6J, which differ in lipofuscin deposition. A comparison of the segregation pattern of cardiac lipofuscin with the albino locus (c) on mouse chromosome 7 revealed complete concordance. Analysis of spontaneous mutants of the tyrosinase gene, encoded by the albino locus, confirmed that the tyrosinase gene itself controls lipofuscin formation. Genetic analysis of other strains indicated that one or more additional genes can contribute to the inheritance of lipofuscin. We also present evidence for an association between cardiac lipofuscin deposition and aortic fatty streak development in the mouse. (J. Clin. Invest. 1993. 92:2386-2393

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Involvement of the tyrosinase gene in the deposition of cardiac lipofuscin in mice. Association with aortic fatty streak development.

Qiao

Welch²,

Xie³

et al. 1993

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…An increasing number of cells containing lipofuscin-like pigments were detected 4 hours after the last DNR injection (Figure 2C). Elevated levels of lipofuscin-like pigments have been found in the spleen of mice subjected to ionising radiation [18], and could be due to accumulation of non-degradable debris in for instance macrophages [19]. The number of cells positive for lipofuscin-like pigments decreased during the next 20 hours (Figure 2C), as was seen for pyknosis and TUNEL-positive cells (Figure 2A).…”

Section: Resultsmentioning

confidence: 86%

Functional p53 is required for rapid restoration of daunorubicin-induced lesions of the spleen

et al. 2013

View full text Add to dashboard Cite

BackgroundThe tumour suppressor and transcription factor p53 is a major determinant of the therapeutic response to anthracyclines. In healthy tissue, p53 is also considered pivotal for side effects of anthracycline treatment such as lesions in haematopoietic tissues like the spleen. We used a Trp53null mouse to explore the significance of p53 in anthracycline (daunorubicin) induced lesions in the spleen.MethodsMice with wild type or deleted Trp53 were treated with the daunorubicin (DNR) for three consecutive days. Spleens were collected at various time points after treatment, and examined for signs of chemotherapy-related lesions by microscopic analysis of haematoxylin-eosin or tunel-stained paraffin sections. Expression of death-inducing proteins was analysed by immunoblotting. Changes between Trp53 wild type and null mice were compared by t-tests.ResultsSigns of cell death (pyknotic nuclei and tunel-positive cells) in the white pulp of the spleen occurred earlier following DNR exposure in wt-mice compared to Trp53-null mice. While the spleen of wt-mice recovered to normal morphology, the spleen of the Trp53-null animals still had lesions with large necrotic areas and disorganised histologic appearance eight days after treatment. Immunoblotting showed that only Trp53-wt mice had significant increase in p21 after DNR treatment. However, both wt and null mice had elevated p63 levels following DNR exposure.Conclusionsp53 protects against severe and enduring cellular damage of the spleen parenchyma after DNR treatment, and initial DNR-induced apoptosis is not predictive of tissue lesions in the spleen. Our data indicate that p53 induction following DNR treatment serves to protect rather than to destroy normal tissue.

show abstract

“…About 16 ± 7% of back skin was of black colour indicating anagen/early catagen, while the rest -85% was probably in telogen/late catagen/ early anagen. However, in the skin of old animals the pigmented spots might develop in a similar way as in humans, due to deposition of poorly degraded melanin or lipofuscin (Kent, 1976;Crichton et al, 1978;Goyarts et al, 2007). Therefore -a histological examination of skin was performed to show that, indeed, in old mice various hair follicles were in different stages of hair cycling.…”

Section: Figure 2 Association Of Macroscopic Splenic Melanosis With mentioning

confidence: 99%

“…Some authors identify the melanin-bearing splenic cells as "melanophores" (Van der Heijden et al, 1995) akin to melanocytes. The occurence of splenic melanosis varies between particular reports (10-21%, Weissman, 1967;8-34%, Crichton et al, 1978;15%, Veninga et al, 1989;23%, van der Heijden et al, 1995;14-80%, Plonka et al, 2005b) but rarely exceeds 30% (34% for female C57BL/6J and 31% for female C57BL/IOScSn, Crichton et al, 1978; 50-80% for female C57BL/6 in late catagen/early telogen, Plonka et al, 2005b). As the reason of this pigmentatory effect some authors suggested haemosiderins (Veninga et al, 1989) or lipofuscin (Crichton et al, 1978), but most of them, starting with Weissman (1967) and followed by Sundberg (1991), van der Heijden et al (1995, and recently by us (Plonka et al, 2005b), insist that melanin is the pigment responsible for the phenomenon.…”

Section: Introductionmentioning

confidence: 97%

Extradermal melanin transfer? Lack of macroscopic spleen melanization in old C57BL/6 mice with de-synchronized hair cycle.

Michalczyk

Popik²,

Salwinski³

et al. 2009

Acta Biochim Pol

View full text Add to dashboard Cite

In quest of alternate, extradermal path of melanin transfer from skin to the visceral organs, we suggested that some portions of such melanin may be deposited in the spleen, which in young black C57BL/6 mice is often melanized. Here, we confirm these observation using young C57BL/6 female mice (up to 17 weeks) and show that this phenomenon cannot be observed in old animals where the hair cycle is not synchronized any more. The experiments were carried out both on spontaneous and depilation-induced hair cycle. We have checked it as a side-observation over many other experiments carried out on young and old C57BL/6 female mice (up to 2.5 years of life). The presence or absence of melanin in the spleens was checked macroscopically, and histologically by Fontana-Masson (FM) staining, and synchronization of the hair cycle - by standard histomorphometric analysis of the back skin hair follicles. In about 40% of old spleens black FM-stainable "debris" could be found under closer histological examination. This study shows that, at least in part, the phenomenon of splenic melanosis in C57BL/6 mice can be correlated with the synchronized skin melanization parallel to the hair cycle progress, and that splenic melanin undergoes gradual degradation during the mouse life.

show abstract

Splenic lipofuscinosis in mice

Cited by 16 publications

References 20 publications

Involvement of the tyrosinase gene in the deposition of cardiac lipofuscin in mice. Association with aortic fatty streak development.

Involvement of the tyrosinase gene in the deposition of cardiac lipofuscin in mice. Association with aortic fatty streak development.

Functional p53 is required for rapid restoration of daunorubicin-induced lesions of the spleen

Extradermal melanin transfer? Lack of macroscopic spleen melanization in old C57BL/6 mice with de-synchronized hair cycle.

Contact Info

Product

Resources

About