Role of α<sub>1</sub>-adrenoceptor subtypes on corneal epithelial thickness and cell proliferation in mice

Musayeva, Aytan; Manicam, Caroline; Steege, Andreas; Brochhausen, Christoph; Straub, Beate K.; Bell, Katharina; Pfeiffer, Norbert; Gericke, Adrian

doi:10.1152/ajpcell.00314.2018

Cited by 9 publications

(6 citation statements)

References 39 publications

(41 reference statements)

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“…On the following day, the graft was transferred into a Petri dish and stained as described previously [13]. After a wash in phosphate-buffered saline, the graft was incubated in trypan blue dye 0.4% (GibcoTM Thermo Fisher Scientific Inc., Waltham, MA, USA) for 1 minute.…”

Section: Methodsmentioning

confidence: 99%

How to Avoid an Upside-Down Orientation of the Graft during Descemet Membrane Endothelial Keratoplasty?

Wasielica‐Poslednik

Schuster

Rauch

et al. 2019

Journal of Ophthalmology

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Purpose. Incorrect anterior-posterior orientation of the Descemet endothelial complex (DEC) is one of the causes of failure of Descemet membrane endothelial keratoplasty (DMEK). We evaluated a new marking technique to avoid such a misorientation. Method. A new marking technique of the DEC was evaluated in patients requiring primary DMEK. A Braille-“R”-letter was applied dot by dot onto the stromal surface of the DEC after lifting it by injecting an air-bubble into the interface between the endothelial surface of the partially stripped graft. The positioning of the graft was intraoperatively controlled by an orientation of the Braille-“R”-letter. Laboratory tests were conducted to test the impact of the marking technique on endothelial cell count. Results. We included prospectively 37 eyes of 30 patients. Four eyes were phakic and 33 pseudophakic. Five grafts (14%) presented an undifferentiated rolling tendency in the anterior chamber, and evaluation of their positioning was possible due to orientation of the mark alone. In case of an upside-down orientation, grafts were flipped immediately. A correct orientation of the graft was achieved in all cases at the end of the surgery. The endothelial cell loss due to the mark was estimated to be less than 0.3%. At 3- and 6-month follow-ups, the mean best-corrected visual acuity was 0.21 ± 0.15 and 0.15 ± 0.11 logMAR, respectively, and endothelial cell density was 1661 ± 349 and 1618 ± 396 cells/mm2, respectively. Only one patient (3%) needed re-bubbling. Conclusions. To rely on the natural rolling tendency of the graft alone does not assure its correct positioning in all cases. Creation of the mark with 4 dots punctuated on the air-lifted stromal side of the DEC is a simple and endothelial cell saving marking method to ensure correct orientation of the graft during DMEK.

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Section: Methodsmentioning

confidence: 99%

How to Avoid an Upside-Down Orientation of the Graft during Descemet Membrane Endothelial Keratoplasty?

Wasielica‐Poslednik

Schuster

Rauch

et al. 2019

Journal of Ophthalmology

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“…Tissue sections were viewed and photographed under a fluorescent microscope (Nikon Eclipse E800) equipped with a digital SPOT camera (Nikon Inc., Tokyo, Japan). DAPI- and Ki-67-labelled cells were counted through the entire thickness of the corneal epithelium in a central zone of 880 µm width by a masked evaluator (A.M.) as previously described [ 50 ]. The rate of proliferating cells was defined as the percentage of Ki-67-positive cells of all DAPI-positive cells.…”

Section: Methodsmentioning

confidence: 99%

Aged Mice Devoid of the M3 Muscarinic Acetylcholine Receptor Develop Mild Dry Eye Disease

Musayeva

Jiang

Ruan

et al. 2021

IJMS

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The parasympathetic nervous system is critically involved in the regulation of tear secretion by activating muscarinic acetylcholine receptors. Hence, various animal models targeting parasympathetic signaling have been developed to induce dry eye disease (DED). However, the muscarinic receptor subtype (M1–M5) mediating tear secretion remains to be determined. This study was conducted to test the hypothesis that the M3 receptor subtype regulates tear secretion and to evaluate the ocular surface phenotype of mice with targeted disruption of the M3 receptor (M3R−/−). The experimental techniques included quantification of tear production, fluorescein staining of the ocular surface, environmental scanning electron microscopy, assessment of proliferating cells in the corneal epithelium and of goblet cells in the conjunctiva, quantification of mRNA for inflammatory cytokines and prooxidant redox enzymes and quantification of reactive oxygen species. Tear volume was reduced in M3R−/− mice compared to age-matched controls at the age of 3 months and 15 months, respectively. This was associated with mild corneal epitheliopathy in the 15-month-old but not in the 3-month-old M3R−/− mice. M3R−/− mice at the age of 15 months also displayed changes in corneal epithelial cell texture, reduced conjunctival goblet cell density, oxidative stress and elevated mRNA expression levels for inflammatory cytokines and prooxidant redox enzymes. The findings suggest that the M3 receptor plays a pivotal role in tear production and its absence leads to ocular surface changes typical for DED at advanced age.

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“…Total cornea and stromal thickness measurements were taken from three sections/mouse/group (n = 5 mice/group; 15 sections/group) at three separate intervals in the central cornea using ImageJ Software. 54 Stromal cells were counted using NIH ImageJ multipoint function in three H&E corneal sections/mouse (15 sections) and the average presented graphically.…”

Section: Methodsmentioning

confidence: 99%

PEDF Gene Deletion Disrupts Corneal Innervation and Ocular Surface Function

Shang

Liu

et al. 2021

Invest. Ophthalmol. Vis. Sci.

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Purpose The cornea is richly innervated by the trigeminal ganglion (TG) and its function supported by secretions from the adjacent lacrimal (LG) and meibomian glands (MG). In this study we examined how pigment epithelium–derived factor (PEDF) gene deletion affects the cornea structure and function. Methods We used PEDF hemizygous and homozygous knockout mice to study effects of PEDF deficiency on corneal innervation assessed by beta tubulin staining, mRNA expression of trophic factors, and PEDF receptors by adjacent supporting glands, corneal sensitivity measured using a Cochet-Bonnet esthesiometer, and tear production using phenol red cotton thread wetting. Results Loss of PEDF was accompanied by reduced corneal innervation and sensitivity, increased corneal surface injury and tear production, thinning of the corneal stroma and loss of stromal cells. PEDF mRNA was expressed in the cornea and its supporting tissues, the TG, LG, and MG. Deletion of one or both PEDF alleles resulted in decreased expression of essential trophic support in the TG, LG, and MG including nerve growth factor, brain-derived neurotrophic growth factor, and GDNF with significantly increased levels of NT-3 in the LG and decreased EGF expression in the cornea. Decreased transcription of the putative PEDF receptors, adipose triglyceride lipase, lipoprotein receptor–related protein 6, laminin receptor, PLXDC1, and PLXDC2 was also evident in the TG, LG and MG with the first three showing increased levels in corneas of the Pedf +/ − and Pedf − / − mice compared to wildtype controls. Constitutive inactivation of ERK1/2 and Akt was pronounced in the TG and cornea, although their protein levels were dramatically increased in Pedf − / − mice. Conclusions This study highlights an essential role for PEDF in corneal structure and function and confirms the reported rescue of exogenous PEDF treatment in corneal pathologies. The pleiotropic effects of PEDF deletion on multiple trophic factors, receptors and signaling molecules are strong indications that PEDF is a key coordinator of molecular mechanisms that maintain corneal function and could be exploited in therapeutic options for several ocular surface diseases.

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Role of α₁-adrenoceptor subtypes on corneal epithelial thickness and cell proliferation in mice

Cited by 9 publications

References 39 publications

How to Avoid an Upside-Down Orientation of the Graft during Descemet Membrane Endothelial Keratoplasty?

How to Avoid an Upside-Down Orientation of the Graft during Descemet Membrane Endothelial Keratoplasty?

Aged Mice Devoid of the M3 Muscarinic Acetylcholine Receptor Develop Mild Dry Eye Disease

PEDF Gene Deletion Disrupts Corneal Innervation and Ocular Surface Function

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Role of α1-adrenoceptor subtypes on corneal epithelial thickness and cell proliferation in mice

Cited by 9 publications

References 39 publications

How to Avoid an Upside-Down Orientation of the Graft during Descemet Membrane Endothelial Keratoplasty?

How to Avoid an Upside-Down Orientation of the Graft during Descemet Membrane Endothelial Keratoplasty?

Aged Mice Devoid of the M3 Muscarinic Acetylcholine Receptor Develop Mild Dry Eye Disease

PEDF Gene Deletion Disrupts Corneal Innervation and Ocular Surface Function

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Role of α₁-adrenoceptor subtypes on corneal epithelial thickness and cell proliferation in mice