Müller glial cells from transgenic mice are more resistant to iron-mediated stress than Müller glial cells from wild-type mice

A: Culture of Müller glial (MG) cells from wild-type (WT) and transgenic (Tg) mice at the first passage were treated with 100 µM of FeCl-NTA (FN), during 96 h. The number of cells was evaluated by counting in comparison to control condition. Each column represents the mean ±SEM. The triple asterisk represent statistical significance of differences between treated and control, respectively, for WT and Tg, and between control and treated, p<p><b>Copyright information:</b></p><p>Taken from "The protective role of transferrin in Müller glial cells after iron-induced toxicity"</p><p></p><p>Molecular Vision 2008;14():928-941.</p><p>Published online 20 May 2008</p><p>PMCID:PMC2391081.</p><p></p

Transferrin secretion in medium of Müller glial cells from 8 to 12-day-old wild-type and transgenic mice decreases with the subcultures

A: Mouse transferrin (mTf) secretion in medium of cultured Müller glial (MG) cells from wild-type ( WT) and transgenic (Tg) mice at confluency after primary culture (P0) and at the first (P1) and the second passages (P2) was measured by radioimmunoassay (RIA; ng/ml). Each column represents the mean ±SEM. The asterisk represents statistical significance of differences between WT and Tg at P0, p<p><b>Copyright information:</b></p><p>Taken from "The protective role of transferrin in Müller glial cells after iron-induced toxicity"</p><p></p><p>Molecular Vision 2008;14():928-941.</p><p>Published online 20 May 2008</p><p>PMCID:PMC2391081.</p><p></p

Mouse transferrin and human transferrin proteins expression are modulated after iron stress

A: Mouse transferrin (mTf) secretion was measured by radioimmunoassay (RIA) in the culture medium of Müller glial (MG) cells from wild-type (WT) and transgenic (Tg) mice in control condition or after addition of 100 µM of FeCl-NTA (FN) during 96 h. Each column represents the mean ±SEM. The double asterisk represents statistical significance of differences between treated and control, respectively, for WT and Tg, p<p><b>Copyright information:</b></p><p>Taken from "The protective role of transferrin in Müller glial cells after iron-induced toxicity"</p><p></p><p>Molecular Vision 2008;14():928-941.</p><p>Published online 20 May 2008</p><p>PMCID:PMC2391081.</p><p></p

Confocal microscopy (CM) and SHG microscopy imaging of the DM from control and diabetic rat corneas.

<p>Unstained intact rat cornea observed by (a and c) <i>in vivo</i> CM and (b, d–i, j) <i>ex vivo</i> SHG microscopy detected in the (e) backward direction and in the (b,d,i–j) forward direction : (b-e) frontal optical sections, (i) 3D view and (j) transverse numerical reconstruction of the DM (image size: 108×108×7 µm³). Intensity profiles from (f) CM, (g) forward-detected and (h) backward-detected SHG microscopy along 100 µm are plotted under the corresponding images. The number of detected photons has been corrected from the channel sensitivity. St: stroma, DM: Descemet’s membrane. White arrows indicate collagen abnormal deposits in the DM. The look-up-table (LUT) used for SHG images is indicated near (b).</p

SHG imaging of the DM from human corneas with different clinical data.

<p>Transverse optical section in the DM (a) from a diabetic donor with unbalanced type 2 diabetes, (b) from a diabetic donor with balanced type 2 diabetes, (c) from a donor with hypertension and (d) from a donor without clinical data related to hyperglycemia or hypertension.</p

Multimodal imaging of histological sections from the same diabetic rat cornea.

<p>(a–c) Frontal and (d–f) transverse histological sections of the cornea observed (a, d) by transmitted light microcopy, (b, c and e) by TEM, where insets show long-spacing collagen, and (f) by SHG microscopy. St: stroma, DM: Descemet’s membrane. White arrows indicate collagen abnormal deposits in the DM.</p

Diabetic and control rat corneas: clinical data and observations by SHG microscopy and other imaging techniques.

<p>Grading is as follows: N/A: not available, −: absence of fibrillar collagen, +: few fibrillar collagen, ++: great concentration of fibrillar collagen, +++: fibrillar collagen over the whole field of view.</p

Methodology to compare the different imaging techniques on rat and human corneas.

<p>Cornea preparation, orientation of the different histological and numerical sections and imaging geometry are indicated for each imaging technique. Histological sections are unstained for SHG microscopy, stained with toluidine blue for transmitted light microscopy and stained with uranyl and lead citrate solutions for transmission electron microscopy.</p

Human corneas: clinical data and observations by SHG microscopy and other imaging techniques.

<p>Grading is as follows: N/A: not available, −: absence of fibrillar collagen, +: few fibrillar collagen, ++: great concentration of fibrillar collagen, +++: fibrillar collagen over the whole field of view.</p

Multimodal imaging of the DM from the same diabetic human cornea.

<p>(a–d) Frontal and (e–h) transverse sections. (a, e) SHG microscopy of intact cornea: (a) frontal optical section, (e) transverse numerical reconstruction. (b, f) Transmitted light microcopy of stained histological sections, where the abnormalities are visible with few contrast. (c, d, g) TEM views of (c, g) the entire DM and (d) its posterior part and the endothelium: long-spacing collagen appears to be synthesized by the endothelial cell. (h) SHG imaging of the same transverse histological section, where fibrillar collagen is clearly identified in the DM. St: stroma, ABL: anterior banded layer, PNBL: posterior nonbanded layer, En: endothelium. White arrows indicate collagen abnormal deposits in the DM.</p