Eryn Hassemer, Ph.D.
Associate Professor
- Milwaukee WI UNITED STATES
- Physics and Chemistry
Dr. Eryn Hassemer's areas of expertise include cell biology and biomolecular engineering.
Education, Licensure and Certification
Ph.D.
Cell Biology
Medical College of Wisconsin
2010
B.S.
Human Biology
University of Wisconsin-Green Bay
2003
Biography
Areas of Expertise
Accomplishments
Engineering Unleashed Fellow
2020
BioE 2nd Place Senior Design Poster Award – Team The Broken Hearts
2018
BioE 1st Place Senior Design Poster Award – Team Cardiac Crusaders
2017
Falk Engineering Educator Award, MSOE
2016
BioE 1st and 3rd Place Senior Design Poster Awards – Teams Bravehearts and Bacteria Busters
2016
Falk Engineering Educator Award Finalist
2015
Affiliations
- American Society for Biochemical & Molecular Biology (ASBMB), 2013-Present
- American Society for Engineering Education (ASEE), 2013-Present
- American Institute for Chemical Engineers (AIChE), 2012-Present
- Society for Biological Engineers (SBE), 2011-Present
Media Appearances
Engineering Unleashed Fellow
Milwaukee School of Engineering online
2020-10-28
Dr. Eryn Hassemer, associate professor in the BioMolecular Engineering program within the Physics and Chemistry Department, was named an Engineering Unleashed 2020 Fellow for her contribution to engineering education, specifically entrepreneurial engineering.
Fal Engineering Educator Award
Milwaukee School of Engineering online
2016-09-09
Dr. Eryn Hassemer, assistant professor in the BioMolecular Engineering program within the Physics and Chemistry Department was awarded the Falk Engineering Educator Award. The award is given annually to full-time faculty members with less than seven years experience. It is a testament to exemplary dedication and performance.
Event and Speaking Appearances
Pioneering the Incorporation of Cell Culture in a New Biomolecular Engineering Program
ASEE IL-IN Conference Terre Haute, IN. March 2014
Preparation and Challenges of Initial Accreditation Approval
ASEE IL-IN Conference Terre Haute, IN. March 2014
Transitioning from Post-Doc to a Teaching Faculty Position
Medical College of Wisconsin Milwaukee, WI. June 2013
Mapping and Cloning of the woe Locus
Cell Biology, Neurobiology and Anatomy Defense Milwaukee, WI, March 2010
Waved With Open Eyes (Woe) Phenotype Caused by a Mutation in Adam17
The American Society of Human Genetic November 2008
Research Grants
Engineering Unleashed Fellowship
Milwaukee School of Engineering
2020-2021
Senior Design Team Servacell
Ideadvance Grant
May 2020 - present
Senior Design Team Chrysaor
MSOE Rader School of Business Seed Grant $750
2019-2020
Senior Design Team Avidity
Plexus Grant $500
October 2019 - May 2020
Senior Design Team Avidity
Small Business Innovation Research (SBIR) $1500
October 2019 - May 2020
Senior Design Team Guts and Glory
MSOE Rader School of Business Seed Grant $500
2018-2019
Senior Design Team Avidity
NSF Innovation Corps $1500
March - April 2019
Senior Design Team Fowl Play
MSOE Rader School of Business Seed Grant $500
2017-2018
Senior Design Team Four of Hearts
MSOE Rader School of Business Seed Grant $500
2017-2018
Senior Design Team CODE
MSOE Rader School of Business Seed Grant $500
2017-2018
Senior Design Team Cardiac Crusaders
MSOE Rader School of Business Seed Grant $500
2016-2017
Senior Design Team MIRACLE
MSOE Rader School of Business Seed Grant $500
2016-2017
Selected Publications
Engaging First-year Students in Undergraduate Professional Development
FYEE Conference• Hassemer EL, Afshan GS, Lee JC, Ozturk S and Shaikh F.
August 3, 2015
Undergraduate professional development addresses future employer’s expectations and academic success through the students’ undergraduate experience. The unique BioMolecular Engineering (BioE) program at the Milwaukee School of Engineering (MSOE) implemented a novel sequence of four seminar courses, BioMolecular Engineering Seminar I-IV. These courses promote the professional development of BioE students from freshman through senior years. The overall goal is for the students to attain a broad understanding of their future profession as well as provide an atomosphere that reinforces the links between their academic learning and professional opportunities available to them post- graduation. All four seminar courses are focused on student participation and led by a team of four faculty members working together in planning and recruiting a wide variety of speakers – educators, engineers, researchers, and entrepreneurs. The students are exposed to multiple academic and industrial projects given by the semina
Career imperative. Is it legal? Is it ethical?
Conference Proceedings of the IEEE Engineering in Medicine and Biology SocietyCohen, B., Fennigkoh, L., Borowicz, J., Hassemer, L.
2014
This paper gives sample ethical case vignettes and discussions that will be presented at the 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC'14) special session of the Ethics and Professional Responsibility Committee. The session includes additional cases with audience participation and panel discussions.
ADAM17 Transactivates EGFR Signaling during Embryonic Eyelid Closure
Investigative Ophthalmology & Visual ScienceHassemer EL, Endres B, Toonen JA, Ronchetti A, Dubielzig R, Sidjanin DJ
2012
PURPOSE:
During mammalian embryonic eyelid closure ADAM17 has been proposed to play a role as a transactivator of epidermal growth factor receptor (EGFR) signaling by shedding membrane bound EGFR ligands. However, ADAM17 also sheds numerous other ligands, thus implicating ADAM17 in additional molecular pathways. The goal of this study was to experimentally establish the role of ADAM17 and determine ADAM17-mediated pathways essential for the embryonic eyelid closure.
METHODS:
Wild-type (WT) and woe mice, carrying a hypomorphic mutation in Adam17, were evaluated using H&E and scanning electron microscopy. Expressions of ADAM17, EGFR, and the phosphorylated form EGFR-P were evaluated using immunohistochemistry. BrdU and TUNEL assays were used to evaluate cell proliferation and apoptosis, respectively. In vitro scratch assays of primary cultures were used to evaluate cell migration. Clinical and histologic analyses established if the hypermorphic Egfr(Dsk5) allele can rescue the woe embryonic eyelid closure.
RESULTS:
woe mice exhibited a failure to develop the leading edge of the eyelid and consequently failure of the embryonic eyelid closure. Expression of ADAM17 was identified in the eyelid epithelium in the cells of the leading edge. ADAM17 is essential for epithelial cell migration, but does not play a role in proliferation and apoptosis. EGFR was expressed in both WT and woe eyelid epithelium, but the phosphorylated EGFR-P form was detected only in WT. The Egfr(Dsk5) allele rescued woe eyelid closure defects, but also rescued woe anterior segment defects and the absence of meibomian glands.
CONCLUSIONS:
We provide in vivo genetic evidence that the role of ADAM17 during embryonic eyelid closure is to transactivate EGFR signaling.
The waved with open eyelids (woe) locus is a hypomorphic mouse mutation in Adam17
GeneticsHassemer, E.L., Le Gall, S.M., Liegel, R., McNally, M., Chang, B., Zeiss, C.J., Dubielzig, R.D., Horiuchi, K., Kimura, T., Okada, Y., Blobel, C.P.
2010
The waved with open eyes (woe) locus is a spontaneous recessive mouse mutation that exhibits wavy fur, eyelids open at birth, and enlarged heart and esophagus. In this study, we confirmed the previously identified woe phenotypes and additionally identified anterior eye segment defects, absence of the meibomian glands, and defects in the semilunar cardiac valves. Positional cloning identified a C794T substitution in the Adam17 gene that ablates a putative exonic splicing enhancer (ESE) sequence in exon 7 resulting in aberrant Adam17 splicing. The predominant woe transcript, Adam17(Delta)(exon7), lacks exon 7 resulting in an in-frame deletion of 90 bp and a putative Adam17(Delta252-281) protein lacking residues 252-281 from the metalloprotease domain. Western blot analysis in woe identified only the precursor form of Adam17(Delta252-281) protein. Absence of cleavage of the prodomain renders Adam17(Delta252-281) functionally inactive; however, constitutive and stimulated shedding of Adam17 substrates was detected in woe at significantly reduced levels. This residual Adam17 shedding activity in woe most likely originates from full-length Adam17(T265M) encoded by the Adam17(C794T) transcript identified expressed at severely reduced levels. These results show that even small amounts of functional Adam17 allow woe mice to survive into adulthood. In contrast to Adam17(-/-) mice that die at birth, the viability of woe mice provides an excellent opportunity for studying the role of Adam17 throughout postnatal development and homeostasis.
Genetic and clinical evaluation of juvenile retinoschisis
Journal of AAPOS: The Official Publication of the American Association for Pediatric Ophthalmology and Strabismus / American Association for Pediatric Ophthalmology and StrabismusKim, J.E., Ruttum, M.S., Koeberl, M.J., Hassemer, E.L., Sidjanin, D.J.
2009
Juvenile retinoschisis is a rare retinal dystrophy caused by RS1 gene mutations.(1) Clinical examinations and molecular testing definitively diagnosed juvenile retinoschisis in 2 male infants, one of whom had a novel mutation not previously reported in the United States. Genetic testing may be the simplest way to confirm this diagnosis in infants.
Production of NAADP and its role in Ca2+ mobilization associated with lysosomes in coronary arterial myocytes
American Journal of Physiology-Heart and Circulatory PhysiologyZhang, F., Zhang, G., Zhang, A.Y., Koeberl, M.J., Wallander, E. Li, P.L
2006
The present study was designed to determine the production of nicotinic acid adenine dinucleotide phosphate (NAADP) and its role associated with lysosomes in mediating endothelin-1 (ET-1)-induced vasoconstriction in coronary arteries. HPLC assay showed that NAADP was produced in coronary arterial smooth muscle cells (CASMCs) via endogenous ADP-ribosyl cyclase. Fluorescence microscopic analysis of intracellular Ca2+ concentration ([Ca2+]i) in CASMCs revealed that exogenous 100 nM NAADP increased [Ca2+]i by 711 ± 47 nM. Lipid bilayer experiments, however, demonstrated that NAADP did not directly activate ryanodine (Rya) receptor Ca2+ release channels on the sarcoplasmic reticulum. In CASMCs pretreated with 100 nM bafilomycin A1 (Baf), an inhibitor of lysosomal Ca2+ release and vacuolar proton pump function, NAADP-induced [Ca2+]i increase was significantly abolished. Moreover, ET-1 significantly increased NAADP formation in CASMCs and resulted in the rise of [Ca2+]i in these cells with a large increase in global Ca2+ level of 1,815 ± 84 nM. Interestingly, before this large Ca2+ increase, a small Ca2+ spike with an increase in [Ca2+]i of 529 ± 32 nM was observed. In the presence of Baf (100 nM), this ET-1-induced two-phase [Ca2+]i response was completely abolished, whereas Rya (50 μM) only markedly blocked the ET-1-induced large global Ca2+ increase. Functional studies showed that 100 nM Baf significantly attenuated ET-1-induced maximal constriction from 82.26 ± 4.42% to 51.80 ± 4.36%. Our results suggest that a lysosome-mediated Ca2+ regulatory mechanism via NAADP contributes to ET-1-induced Ca2+ mobilization in CASMCs and consequent vasoconstriction of coronary arteries.
