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Erythropoietin (EPO) is a glycoprotein hormone that stimulates the production of erythrocytes in red bone marrow. Although EPO is primarily produced and released by the kidneys in response to low tissue levels of oxygen, several other tissues, including the liver and neurons of the central nervous system (CNS), can produce EPO. EPO binds the EPO receptor (EPOR) in erythrocyte precursor cells, causing them to differentiate into mature erythrocytes that are released into circulation. As the oxygen-carrying capacity of the blood increases, secretion of EPO by the kidneys decreases. Neurons in the CNS also express EPOR, and EPO has been shown to decrease apoptosis of both erythrocyte precursor cells and CNS neurons. EPO also promotes angiogenesis, the production of new blood vessels. The human EPO gene has been cloned and expressed in vitro. The recombinant gene product (rHuEPO) is frequently administered to patients who have anemia resulting from either kidney failure or chemotherapy. More recently, it has been shown that a significant number of tumors express EPOR, even though the healthy tissue from which the tumor was derived does not. Experiments in mice indicate that EPO prevents apoptosis and increases angiogenesis in at least some types of EPOR-positive tumors. Interested in developing ways to treat human strokes, researchers are attempting to develop forms of EPO that act on CNS neurons without affecting erythrocyte production in the bone marrow. One benefit of such a form of EPO in stroke treatment would be to: O A. promote apoptosis of damaged CNS neurons without affecting blood oxygen levels. O B. limit neuronal cell death without causing an immediate decrease in the oxygen-carrying capacity of the blood. O C. prevent apoptosis in the CNS without causing a harmful increase in blood viscosity. O D. promote healing in the CNS without increasing the risk of developing tumors.

by | Sep 8, 2023 | biology

Erythropoietin (EPO) is a glycoprotein hormone that stimulates
the production of erythrocytes in red bone marrow. Although EPO is
primarily produced and released by the kidneys in response to low
tissue levels of oxygen, several other tissues, including the liver and
neurons of the central nervous system (CNS), can produce EPO.
EPO binds the EPO receptor (EPOR) in erythrocyte precursor cells,
causing them to differentiate into mature erythrocytes that are
released into circulation. As the oxygen-carrying capacity of the
blood increases, secretion of EPO by the kidneys decreases.
Neurons in the CNS also express EPOR, and EPO has been shown
to decrease apoptosis of both erythrocyte precursor cells and CNS
neurons. EPO also promotes angiogenesis, the production of new
blood vessels. The human EPO gene has been cloned and
expressed in vitro. The recombinant gene product (rHuEPO) is
frequently administered to patients who have anemia resulting
from either kidney failure or chemotherapy.
More recently, it has been shown that a significant number of
tumors express EPOR, even though the healthy tissue from which
the tumor was derived does not. Experiments in mice indicate that
EPO prevents apoptosis and increases angiogenesis in at least
some types of EPOR-positive tumors.
Interested in developing ways to treat human strokes, researchers
are attempting to develop forms of EPO that act on CNS neurons
without affecting erythrocyte production in the bone marrow. One
benefit of such a form of EPO in stroke treatment would be to:
O A. promote apoptosis of damaged CNS neurons without
affecting blood oxygen levels.
O B. limit neuronal cell death without causing an immediate
decrease in the oxygen-carrying capacity of the blood.
O C. prevent apoptosis in the CNS without causing a harmful
increase in blood viscosity.
OD. promote healing in the CNS without increasing the risk of
developing tumors.
Expression of the rHuEPO gene in E. coli bacteria produced an EPO
protein that did not increase erythrocyte production when injected
into humans. The most likely reason for this observation is that:
O A. prokaryotic ribosomes interpret the genetic code in a
completely different manner than do eukaryotic
ribosomes.
O B. E. coli cannot glycosylate EPO in the same way that it is
glycosylated by eukaryotic cells.
O C. bacteria are unable to secrete eukaryotic proteins.
OD. only viruses contain the necessary cellular machinery to
properly express recombinant proteins.
Assume that a certain dominant mutation in the EPO gene exists
such that a person who carries this mutant EPO allele has a higher-
than-normal number of circulating erythrocytes. Which of the
following best describes a mechanism by which this mutation
I could have its effect?
OA. The promoter of the mutant EPO allele is defective, and
the allele is not transcribed.
OB. The mutant EPO allele produces a protein that has an
increased affinity for EPOR.
O C. The mRNA produced by the mutant EPO allele is
degraded before translation can occur.
O D. The mutant EPO allele produces a protein that is unable
to bind EPOR.
In which of the following cellular locations does EPO most likely
initially bind EPOR in erythrocyte precursor cells?
O A. Cytosol
OB. Endoplasmic reticulum
O C. Nucleus
O D. Plasma membrane
Certain types of kidney tumors continuously produce and release
EPO. Such tumors most likely have which of the following effects, if
any, on erythrocyte production?
O A. The liver will take over the process of regulating
erythrocyte production.
O B. Erythrocyte production within the bone marrow will
cease.
OC. Constant stimulation of erythrocyte production will occur
within the bone marrow.
OD. There is no effect; erythrocyte production will continue to
be regulated by the kidneys based on oxygen levels
within the body.
An increase in which of the following physiological variables is
most likely to cause an increase in the amount of EPO released by
the kidneys in a healthy human adult?
O A. Amount of aerobic exercise the person performs
OB. Total amount of circulating hemoglobin
Rate of erythrocyte maturation
O C.
O D. Cardiac output (volume of blood pumped by the heart per
minute)
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Transcribed Image Text:Erythropoietin (EPO) is a glycoprotein hormone that stimulates
the production of erythrocytes in red bone marrow. Although EPO is
primarily produced and released by the kidneys in response to low
tissue levels of oxygen, several other tissues, including the liver and
neurons of the central nervous system (CNS), can produce EPO.
EPO binds the EPO receptor (EPOR) in erythrocyte precursor cells,
causing them to differentiate into mature erythrocytes that are
released into circulation. As the oxygen-carrying capacity of the
blood increases, secretion of EPO by the kidneys decreases.
Neurons in the CNS also express EPOR, and EPO has been shown
to decrease apoptosis of both erythrocyte precursor cells and CNS
neurons. EPO also promotes angiogenesis, the production of new
blood vessels. The human EPO gene has been cloned and
expressed in vitro. The recombinant gene product (rHuEPO) is
frequently administered to patients who have anemia resulting
from either kidney failure or chemotherapy.
More recently, it has been shown that a significant number of
tumors express EPOR, even though the healthy tissue from which
the tumor was derived does not. Experiments in mice indicate that
EPO prevents apoptosis and increases angiogenesis in at least
some types of EPOR-positive tumors.
Interested in developing ways to treat human strokes, researchers
are attempting to develop forms of EPO that act on CNS neurons
without affecting erythrocyte production in the bone marrow. One
benefit of such a form of EPO in stroke treatment would be to:
O A. promote apoptosis of damaged CNS neurons without
affecting blood oxygen levels.
O B. limit neuronal cell death without causing an immediate
decrease in the oxygen-carrying capacity of the blood.
O C. prevent apoptosis in the CNS without causing a harmful
increase in blood viscosity.
OD. promote healing in the CNS without increasing the risk of
developing tumors.
Expression of the rHuEPO gene in E. coli bacteria produced an EPO
protein that did not increase erythrocyte production when injected
into humans. The most likely reason for this observation is that:
O A. prokaryotic ribosomes interpret the genetic code in a
completely different manner than do eukaryotic
ribosomes.
O B. E. coli cannot glycosylate EPO in the same way that it is
glycosylated by eukaryotic cells.
O C. bacteria are unable to secrete eukaryotic proteins.
OD. only viruses contain the necessary cellular machinery to
properly express recombinant proteins.
Assume that a certain dominant mutation in the EPO gene exists
such that a person who carries this mutant EPO allele has a higher-
than-normal number of circulating erythrocytes. Which of the
following best describes a mechanism by which this mutation
I could have its effect?
OA. The promoter of the mutant EPO allele is defective, and
the allele is not transcribed.
OB. The mutant EPO allele produces a protein that has an
increased affinity for EPOR.
O C. The mRNA produced by the mutant EPO allele is
degraded before translation can occur.
O D. The mutant EPO allele produces a protein that is unable
to bind EPOR.
In which of the following cellular locations does EPO most likely
initially bind EPOR in erythrocyte precursor cells?
O A. Cytosol
OB. Endoplasmic reticulum
O C. Nucleus
O D. Plasma membrane
Certain types of kidney tumors continuously produce and release
EPO. Such tumors most likely have which of the following effects, if
any, on erythrocyte production?
O A. The liver will take over the process of regulating
erythrocyte production.
O B. Erythrocyte production within the bone marrow will
cease.
OC. Constant stimulation of erythrocyte production will occur
within the bone marrow.
OD. There is no effect; erythrocyte production will continue to
be regulated by the kidneys based on oxygen levels
within the body.
An increase in which of the following physiological variables is
most likely to cause an increase in the amount of EPO released by
the kidneys in a healthy human adult?
O A. Amount of aerobic exercise the person performs
OB. Total amount of circulating hemoglobin
Rate of erythrocyte maturation
O C.
O D. Cardiac output (volume of blood pumped by the heart per
minute)
  

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