St Paul’s Eye Appeal fundraising dinner

Last week St Paul’s eye unit and the Department of Eye and Vision Science at the University of Liverpool hosted a dinner at Liverpool town hall to promote the St Paul’s Eye Appeal. This appeal supports a number of research projects that don’t fit into the common funding mechanisms. i.e. the appeals fills the gap between the research supported by the big research councils and the clinical services supported by the NHS.


Liverpool Town Hall 

In practical terms it makes a massive difference to our department; allowing for strategic investment in people, projects and equipment to push forward new research ideas and get them into the clinic.

It was a great night with a fantastic locally sourced food,


The £1 million dining table, no drink rings please!

wine and gin and really good company. Lots of valuable connections were made and hopefully this will translate into investments into eye research in Liverpool.

The dinner was hosted by Lady Grantchester and amongst the other notable dignitaries  was Stephanie Slater MBE, the paralympic athlete who recently had a corneal transplant at St Paul’s. Not my usual company (!) but a really interesting experience for all involved.

Here are a few photos from the night and select ones involving some of the EVS team below.




Eye eye eye?


Putting together the images from our sunscreen project to prepare the manuscript…. Here are a bunch of the eye images that MRes student Kareem took.

Not sure why but I find it strangely compelling so thought I would share. If you were part of the study I challenge you to spot yourself…

Can’t wait for the paper? The abstract was selected for oral presentation at the British Association of Dermatologists meeting in June, so you will be able to see Kareem in action there.

Lung Fibrosis Studentship Available in Hamill lab

We are pleased to announce we have been awarded funding do a really cool project in the area of matrix assembly in the alveolar epithelium and are currently accepting applications for a funded PhD studentship position. Interested? apply here;

Determination of the mechanisms through which age and disease associated alveolar epithelial matrix changes drive development and progression of pulmonary fibrosis.

Pulmonary fibrosis is a major clinical problem with massive financial and morbidity implications. Importantly, once a fibrotic extracellular matrix (ECM) is formed it currently cannot be reversed, moreover, disease progression continues with the fibrotic matrix shown to induce further profibrotic responses and even exposure to “old” ECM is sufficient to drive changes to matrix protein production and increase the risk of developing pulmonary fibrosis.

Unlike many other matrices, the alveolar ECM is exposed to stretch, with forces increasing. Accumulating evidence point to a critical role for the alveolar basement membrane (BM) in stretch responses, specifically to the importance of laminins (LM) in normal and pathological lung function. It has been shown that LMα 3 expression decreases with and is frequently lost in patients with pulmonary fibrosis, while other LMs expression is dysregulated in scleroderma associated lung fibrosis. Alveolar epithelial cell (AEC) LMα 3 knockout animals display increased fibrosis and mortality in the bleomycin fibrotic but is against overextension in ventilator induced lung injury models. Interestingly, whereas LMs are organized in cloud like arrays in matrix of skin/corneal epithelial cells, in AECs they assembles into fibrillar arrays (figure) and LMα 3 has been shown to stretch signal via a complex containing nidogen, perlecan, and dystroglycan.


Laminin network assembly responds to stretch. Left; skin epithelial cells, Right; alveolar epithelial cells exposed to cyclic stretch, both stained with antibodies against laminin alpha3 (Hamill et al. JCS 2009)

However, surprisingly little is known about how alveolar epithelial cells assemble their BM; how the LM assembles differently under stretch, the effect on other BM components of changing the LM matrix, the effect of age-associated changes to the ECM and how those changes lead to fibrosis susceptibility is yet to be investigated. This studentship will use in vitro models and scleroderma patient samples to answer these questions.

To answer these questions this studentship will use in vitro stretch models of alveolar epithelial cells in 2D and 3D culture along with pulmonary fibroblasts along with a variety of cell and molecular approaches. These will include high end techniques such as mass spectroscopy, genome editing, and live cell/molecular imaging modalities including superresolution microscopy and atomic force microscopy.

The student undertaking these studies will benefit from a diverse supervisory team each bringing valuable skills to the project. The studentship will take place primarily in the custom built laboratories of the Institute of Ageing and Chronic Disease at the University which opened in 2016. You will also join a team of scientists investigating different questions relating to pulmonary fibrosis and stretch signalling.

The Institute of Ageing and Chronic Disease is fully committed to promoting gender equality in all activities. In recruitment we emphasize the supportive nature of the working environment and the flexible family support that the University provides. The Institute holds a silver Athena SWAN award in recognition of on-going commitment to ensuring that the Athena SWAN principles are embedded in its activities and strategic initiatives.


At minimum applicants should hold or expect to obtain a 1st class or upper second class undergraduate degree or a masters level qualification within biochemistry, molecular or cellular biology disciplines or related fields. Preference will be given to students with extensive lab experience.

Want to know more about the lab/institute:

Lab website:

Institute Website:

Funding Notes

This is a funded studentship supported by an endowment to the University of Liverpool. This will provide a stipend, fees at the UK/EU rate and a consumables budget


Laminin deposition in the extracellular matrix: a complex picture emerges.
Hamill KJ, Kligys K, Hopkinson SB, Jones JC.
J Cell Sci. 2009 Dec 15;122(Pt 24):4409-17. doi: 10.1242/jcs.041095.

Lung-specific loss of α3 laminin worsens bleomycin-induced pulmonary fibrosis.
Morales-Nebreda LI, Rogel MR, Eisenberg JL, Hamill KJ, Soberanes S, Nigdelioglu R, Chi M, Cho T, Radigan KA, Ridge KM, Misharin AV, Woychek A, Hopkinson S, Perlman H, Mutlu GM, Pardo A, Selman M, Jones JC, Budinger GR.
Am J Respir Cell Mol Biol. 2015 Apr;52(4):503-12. doi: 10.1165/rcmb.2014-0057OC.

Lung-specific loss of the laminin α3 subunit confers resistance to mechanical injury.
Urich D, Eisenberg JL, Hamill KJ, Takawira D, Chiarella SE, Soberanes S, Gonzalez A, Koentgen F, Manghi T, Hopkinson SB, Misharin AV, Perlman H, Mutlu GM, Budinger GR, Jones JC.
J Cell Sci. 2011 Sep 1;124(Pt 17):2927-37. doi: 10.1242/jcs.080911.