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1.
Figure 8.

Figure 8. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

Hair density (bars filled with dots) and full skin thickness (bars with diagonal lines) in male (M) and female (F) transgenic mice expressing progerin (K14-progerin), transgenic mice expressing wild-type human lamin A (K14-lamin A) and non-transgenic mice (WT) on Lmna−/−, Lmna+/− and Lmna+/+ backgrounds. Hair density and skin thickness were scored on a scale of 1 (lowest) to 5 (highest). Values are means ± SD for n = 5 to 6 mice. Lmna−/− mice expressing either progerin or wild-type lamin A or without a transgene had significantly decreased hair density and full-skin thickness compared to Lmna+/− and Lmna+/+ mice.

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.
2.
Figure 3.

Figure 3. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

(A) Immunoblotting demonstrating transgene expression in cultured keratinocytes isolated from transgenic mice expressing FLAG-progerin and FLAG-wild-type lamin A. Blots were probed with mouse anti-FLAG (FLAG) and mouse anti-actin (ß-actin) antibodies. Lanes numbered 361, 571, 777 and 796 are from two transgenic mouse lines containing the FLAG-progerin transgene (K14-progerin) and lanes numbered 763, 787, 660 and 851 are from two transgenic mouse lines with the FLAG-wild-type human lamin A transgene; wt indicates proteins extracted from skin of a non-transgenic littermate. (B) Confocal immunofluorescence micrographs of cultured mouse keratinocytes expressing FLAG-progerin (K14-progerin; panels a and d), FLAG-wild-type human lamin A transgene (K14-lamin A; panels b and e) and a non-transgenic littermate (WT littermate; panels c and f). Panels a, b and c show double labeling with anti-FLAG (green) and anti-keratin 14 (red) primary antibodies. For panels d, e and f, cells were labeled with anti-FLAG (green) and anti-lamin A/C (red) antibodies and overlay (yellow) of signals are shown. Bar: 10 µm.

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.
3.
Figure 6.

Figure 6. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

(A) Photographs of sections of dorsal skin from transgenic mice expressing progerin (K14-progerin) or wild-type human lamin A (K14-lamin A) 1 day (d1), 7 days (d7), 10 days (d10) and 13 days (d13) after depilation. Bar: 0.5 cm. (B) Confocal immunohistofluorescence micrographs of dorsal skin sections from transgenic mice expressing progerin (K14-progerin) or wild-type human lamin A (K14-lamin A) 21 days after depilation. Panels show signals using anti-FLAG antibodies (a, g; green), anti-lamin A antibodies (d, j; green), anti-keratin 14 (K14) antibodies (b, h, e, k; red). Merge (c, i, f, l) shows overlay (yellow) of anti-FLAG or anti-lamin A and anti-K14 signals of panels immediately to the left. Bars: 50 µm. (C) Representative sections of skin 21 days after depilation from transgenic mice expressing progerin (K14-progerin) or wild-type human lamin A (K14-lamin A) stained with hematoxylin and eosin showing no significant differences. Bar: 50 µm.

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.
4.
Figure 2.

Figure 2. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

(A) Electron micrographs of epidermal keratinocyte nuclei in skin sections from transgenic mice expressing progerin (K14-progerin; a, b, e, f, i, j) or wild-type human lamin A (K14-lamin A; c, g, k). Sections from non-transgenic controls (WT littermate; d, h, l) are also shown. Arrowhead shows a nuclear pseudoinclusion (j). Bars: 2 µm. (B) Nuclear circularity expressed as contour ratio from different transgenic mouse lines. WT1 and WT2 are results for non-transgenic wild-type littermates; line 50, line 60 and line 79 (K14-progerin) are results for three different transgenic lines expressing progerin; line 28-1 and line 28-2 (K14-lamin A) are results for two different transgenic mice from a line expressing wild-type human lamin A. Values are means ± SD for n = 5–19 nuclei measured. Contour ratios of keratinocyte nuclei in mice expressing progerin were significantly less (*P < 0.01) than those in non-transgenic wild-type littermates or mice expressing wild-type human lamin A. (C) Coefficients of variation for contour ratios of keratinocyte nuclei in B.

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.
5.
Figure 7.

Figure 7. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

(A) Rates of wound healing in transgenic mice expressing progerin or wild-type human lamin A in epidermis. Graphs show mean percentages of wound closure (y-axis) versus days post wounding (x-axis) for transgenic mice expressing progerin (line 79+), their non-transgenic littermates (line 79−), transgenic mice expressing wild-type human lamin A (line 28+) and their non-transgenic littermates (line 28−). Values are means ± SD for n = 6 wounds in three mice from each group (two wounds per mouse); no differences between groups were significant. (B) Representative sections of skin 11 days after wounding (just prior to complete closure) from transgenic mice expressing progerin (K14-progerin), transgenic mice expressing wild-type human lamin A (K14-lamin A) and a non-transgenic control (WT littermate) stained with hematoxylin and eosin showing no significant differences. Healing skins had thickened epidermis (E) and new hair follicles (HF). Arrowheads show healing wounds. Bar: 50 µm.

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.
6.
Figure 5.

Figure 5. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

(A) Representative confocal immunofluorescence micrographs of cultured keratinocytes expressing FLAG-progerin (K14-progerin) and FLAG-wild-type human lamin A (K14-lamin A) during spontaneous immortalization by continuous subculture. Top panels show cultured keratinocytes expressing progerin and bottom panels cultured keratinocytes expressing wild-type human lamin A at passage 1 (P1), passage 8 (P8) and passage 20 (P20) labeled with anti-FLAG antibodies. Bar: 10 µm. (B) Percentages of primary cultured mouse keratinocytes at passage 1 expressing wild-type human lamin A (LaminA-p) or progerin (Progerin-p) and spontaneously immortalized keratinocytes at passage 20 expressing wild-type human lamin A (LaminA-I) or progerin (Progerin-I) with abnormal nuclear morphology. Nuclei in 200–500 cells in 25 microscopic fields per sample were scored for abnormal morphology (‘rough’ rim fluorescence, nuclear envelope ‘blebs’) versus normal morphology (smooth, mostly circular nuclear rim fluorescence). Values are means ± SD for n = 5 experiments on different cell lines. *P < 0.05 for progerin-expressing primary keratinocytes at passage 1 (Progerin-p) compared to spontaneously immortalized progerin-expressing keratinocytes at passage 20 (Progerin-I).

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.
7.
Figure 4.

Figure 4. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

(A) Representative confocal immunofluorescence micrographs of cultured keratinocytes expressing FLAG-wild-type human lamin A (K14-lamin A) and FLAG-progerin (K14-progerin) after treatment with farnesyltransferase inhibitor BMS-214662 or dimethylsulfoxide vehicle. Top panels (+DMSO) show cells after 48 h of treatment with dimethylsulfoxide and lower panels (+FTI) show cells after 48 h of treatment with BMS-214662 labeled with anti-FLAG antibodies. Bar: 10 µm for four left-most panels at left; 5 µm for two panels at right. (B) Percentages of cultured mouse keratinocytes expressing wild-type human lamin A (Lamin A) or progerin (Progerin) with abnormal nuclear morphology after 48 h of treatment with farnesyltransferase inhibitor (+FTI) or dimethylsulfoxide (+DMSO). Nuclei in 200–500 cells in 25 microscopic fields per sample were scored for abnormal morphology (‘rough’ rim fluorescence, nuclear envelope ‘blebs’) versus normal morphology (smooth, mostly circular nuclear rim fluorescence). Values are means ± SD for n = 4 experiments. *P < 0.05 for progerin-expressing cells +FTI compared to +DMSO. (C) Percentages of cultured mouse keratinocytes expressing wild-type human lamin A (Lamin A) or progerin (Progerin) with intranuclear foci after 48 h of treatment with farnesyltransferase inhibitor (+FTI) or dimethylsulfoxide (+DMSO). Nuclei in 200–500 cells in 25 microscopic fields per sample were scored for the presence of fluorescent nuclear foci. Values are means ± SD for n = 2 experiments. *P < 0.05 for progerin-expressing cells +FTI compared to +DMSO.

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.
8.
Figure 1.

Figure 1. From: Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin.

(A) Minigene constructs used for epidermal expression of wild-type human lamin A and progerin. The constructs contained a K14 promoter and ß-globin intron followed by DNA containing an ATG start codon and a FLAG sequence fused in frame to cDNAs encoding either prelamin A (LMNA) or progerin followed by K14 poly A tail. Major restriction endonuclease sites indicated are E: EcoRI, H: HindIII, S: SphI, X: XbaI. Fragments of 5319 and 5170 base pairs (bp), respectively, for wild-type lamin A and progerin were generated by digestion with EcoRI and SphI and microinjected into pronuclei of fertilized mouse oocytes. Diagram not to scale. (B) Immunoblotting demonstrating transgene expression in mouse skin. Blots were probed with mouse anti-lamin A/C (Lamin A/C), mouse anti-FLAG (FLAG) and mouse anti-actin (ß-actin) antibodies. Lanes numbered 44, 50, 60, 79, 447 are from five transgenic mouse lines containing the FLAG-progerin transgene (K14-progerin) and lanes numbered 28, 93, 995 are from three transgenic mouse lines with the FLAG-wild-type human lamin A transgene (K14-lamin A); WT indicates proteins extracted from skin of a non-transgenic littermate. Note faster migration of FLAG-progerin compared to FLAG-wild-type human lamin A. (C). Confocal immunofluorescence micrographs of dorsal skin sections from transgenic expressing FLAG-progerin (K14-progerin), FLAG-wild-type human lamin A transgene (K14-lamin A) and a non-transgenic littermate (WT-littermate). Panels show signals using anti-FLAG antibodies (a–c; green), anti-lamin B1 (d–f; red). Merge (g–i) shows overlay of anti-FLAG and anti-lamin B1 signals of panels immediately above. Lower panels (j–l) show overlay (yellow) of anti-FLAG and anti-lamin B1 signals of other fields at higher magnification. Bars: 50 µm (a–i) and 10 µm (j–l).

Yuexia Wang, et al. Hum Mol Genet. 2008 August 1;17(15):2357-2369.

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